bims-imicid Biomed News
on Immunometabolism of infection, cancer and immune-mediated disease
Issue of 2025–11–16
37 papers selected by
Dylan Gerard Ryan, Trinity College Dublin



  1. Immunol Rev. 2025 Nov;336(1): e70068
      Dendritic cells (DCs) demonstrate remarkable functional and metabolic heterogeneity that governs the balance between immune tolerance and autoimmune pathogenesis. Under homeostatic conditions, tolerogenic DC subsets maintain immunological equilibrium through distinct metabolic programs and the production of immunoregulatory metabolites, promoting T cell anergy and regulatory T cell (Treg) differentiation. In contrast, autoimmune conditions trigger pathogenic metabolic rewiring, shifting DCs toward glycolysis and enhanced lipid synthesis, which drives DC hyperactivation and breakdown of self-tolerance. This metabolic reprogramming is coordinately regulated by external microenvironmental cues and internal signaling pathways, leading to heterogeneous DC responses in diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and psoriasis. Targeting metabolic regulators offers promising therapeutic strategies to restore immune tolerance and prevent harmful autoimmunity and inflammation. The review highlights the intricate interplay between DC metabolism and function, emphasizing how metabolic heterogeneity underpins their dual roles in immune regulation and autoimmunity. Future exploration of subset-specific metabolic preferences and spatiotemporal metabolic dynamics will facilitate the development of precision immunotherapies for autoimmune diseases.
    Keywords:  autoimmunity; dendritic cell; immune homeostasis; immunometabolism; self‐tolerance
    DOI:  https://doi.org/10.1111/imr.70068
  2. Immunometabolism (Cobham). 2025 Oct;7(4): e00073
       Background: Immunometabolism has emerged as a flourishing field exploring how cellular metabolism regulates immune responses. Peripheral blood mononuclear cells (PBMCs) have so far been the primary sample type used for immunometabolic profiling. However, PBMCs isolation requires large blood volumes, can pose logistic challenges, and requires specialized skills for processing. Thus, using whole blood (WB) samples, which are less technically challenging to process, could serve as a viable alternative for metabolic characterization of circulating immune cell populations. Yet, how well WB immunometabolic profiles match those from PBMCs remains unknown. Therefore, we aimed to compare the immunometabolic profile of WB with that of PBMCs.
    Method: Paired WB and PBMCs samples were collected from six healthy donors. WB was collected in CryoStor®-CS10 medium, while PBMCs were isolated using Ficoll density gradient. Using spectral flow cytometry, we identified immune cell populations and assessed their metabolic states.
    Results: Our findings show an overall high similarity in the immune cell subset frequencies between WB and PBMCs as well as their metabolic profiles. However, differences in the expression of certain metabolic markers were noted in some immune populations. Specifically, glucose transporter 1 levels were higher in CD8+ TEMRA, NKT, and NK cells from PBMCs, while ATP5a levels were higher in naïve CD4+ T cells from WB.
    Conclusions: These results suggest that WB can be an alternative to PBMCs for metabolic profiling of immune cells. Nevertheless, for some specific cell subsets, caution should be taken when comparing immunometabolic data between WB and PBMCs.
    Keywords:  immunometabolic profiling; metabolic markers; metabolism; peripheral blood mononuclear cells; spectral flow cytometry; whole blood
    DOI:  https://doi.org/10.1097/IN9.0000000000000073
  3. Int J Biol Sci. 2025 ;21(14): 6411-6429
      Glycolysis activation plays a critical role in sustaining the proinflammatory phenotype of macrophages, which is key to initiating and advancing liver fibrosis. However, the underlying mechanisms that trigger glycolytic activation and their contribution to inflammation remain poorly understood. In this study, we showed that inhibiting glycolysis markedly suppresses macrophage M1 polarization and alleviates liver inflammation and fibrosis, whereas enhancing glycolysis in hepatic macrophages produces the opposite effect. Additionally, our results demonstrated that glycolytic flux is necessary for activation of the STING/TBK1/IRF3 pathway. Moreover, STING activation was found to reciprocally stimulate glycolysis in macrophages. Mechanistically, we found that ATP generated through glycolysis promotes STING pathway activation and enhances the interferon-dependent immune response. Moreover, activation of IRF3, a downstream transcription factor of STING, upregulates HIF-1α transcription, further driving glycolysis. These findings uncover novel mechanistic links between STING signaling and glycolytic metabolism, emphasizing their coordinated role in promoting macrophage M1 polarization. Together, our data suggest that targeting the interaction between metabolic reprogramming and immune signaling offers an effective therapeutic approach for treating liver fibrosis and cirrhosis.
    Keywords:  glycolysis; innate immune response; liver fibrosis; macrophage
    DOI:  https://doi.org/10.7150/ijbs.115073
  4. Eur J Immunol. 2025 Nov;55(11): e70094
      The metabolic programs of immune cells influence their activation, differentiation, and effector functions. While much of immunometabolism has focused on cell-intrinsic regulation, it is now clear that metabolic activity is profoundly influenced by the surrounding tissue environment. In tumors and other inflammatory settings, immune cells are shaped by nutrient gradients, hypoxia, and immunoregulatory metabolites, factors that are spatially heterogeneous and often poorly captured by traditional methods. This review highlights recent technological advances that enable spatially resolved analysis of immune metabolism, with an emphasis on multimodal integration and cancer as a model system. Mass spectrometry imaging (MALDI, DESI), high-resolution platforms like SIMS, and vibrational imaging approaches such as Raman microscopy enable direct visualization of metabolites in tissue. Transcriptomic and proteomic data can be used to infer metabolic states, and computational models are being developed to integrate these diverse data layers. Together, these technologies are transforming the study of immunometabolism from dissociated cells to the intact tissue context. Key challenges remain in resolution, annotation, and data integration, but spatial immunometabolism holds particular promise for illuminating mechanisms of immune regulation in health and disease.
    Keywords:  antitumor immunity; cellular metabolism; immunometabolism; multiplexed imaging; spatial biology; systems immunology; tumor microenvironment
    DOI:  https://doi.org/10.1002/eji.70094
  5. Virology. 2025 Nov 06. pii: S0042-6822(25)00350-2. [Epub ahead of print]614 110736
      Japanese encephalitis virus (JEV), a causative agent of viral encephalitis, manipulates host metabolic pathways to support its replication in the host cells. Glycolysis is one of the crucial metabolic pathways regulated by most of the RNA viruses. In the current study, we investigated the regulation of glycolysis by JEV in Neuro-2a cells. JEV replication induces a time-dependent increase in glycolysis, demonstrated by decreased glucose and elevated lactic acid levels in the supernatant of infected cells. Furthermore, treatment with glycolytic inhibitors, such as 2-Deoxy-D-glucose and sodium oxamate, reduced virus replication. Moreover, supplementation with sodium pyruvate, an alternate energy source, and treatment with insulin promoted JEV replication, highlighting their positive role during metabolic stress in JEV-infected cells. JEV replication also enhanced the expression of several glycolytic enzymes. We identified hypoxia-inducible factor-1α (HIF-1α) as a critical regulator of glycolysis during JEV infection. JEV infection resulted in HIF-1α upregulation, indicating its role in replication kinetics. Cobalt chloride-induced stabilization of HIF-1α enhanced JEV replication, while its knockdown abrogated this effect in treated cells. Altogether, our results reveal that JEV modulates host glucose metabolism via HIF-1α to facilitate its replication and also highlight glycolytic inhibitors as potential antiviral against JEV.
    Keywords:  2-Deoxy-D-glucose; Glycolysis; Hypoxia-inducible factor 1α; Japanese encephalitis virus; Sodium oxamate
    DOI:  https://doi.org/10.1016/j.virol.2025.110736
  6. Mater Today Bio. 2025 Dec;35 102465
      Sepsis persists as a life-threatening clinical syndrome associated with alarmingly high mortality rates, while existing therapeutic strategies demonstrate suboptimal efficacy, necessitating the development of novel interventions. In this study, we engineered pH-responsive nanoparticles (NPs) through an innovative one-pot synthesis utilizing FDA-approved poly-L-lysine (PLL) and cinnamaldehyde (CA), followed by hydrophilic-hydrophobic self-assembly with DSPE-PEG3400. The resulting NPs efficiently encapsulated the glucose transporter 1 (GLUT1) inhibitor BAY-876 (BAY-876@NPs) and exhibited microenvironment responsive drug release kinetics, wherein acidic inflammatory conditions induced protonation of BAY-876@NPs, facilitating controlled drug liberation. In both cecal ligation and puncture (CLP) and lipopolysaccharide (LPS) induced sepsis mice, BAY-876@NPs demonstrated pH-dependent release of BAY-876, effectively attenuating GLUT1 mediated glucose uptake in macrophages. This mechanism concomitantly suppressed lactic acid accumulation and glycolytic flux, thereby reducing pro-inflammatory M1 phenotypes while augmenting anti-inflammatory M2 phenotypes. Consequently, BAY-876@NPs profoundly mitigated systemic inflammation, ameliorated multi-organ dysfunction, and significantly enhanced survival outcomes in septic mice. In summary, BAY-876@NPs exhibit superior biocompatibility and exert potent immunomodulatory effects by selectively inhibiting glycolysis, culminating in robust anti-inflammatory and organ-protective efficacy. These findings position BAY-876@NPs as a promising nanotherapeutic candidate for sepsis management.
    Keywords:  BAY-876; Glycolysis inhibition; Macrophage reprogramming; Sepsis treatment; pH-responsive nanoparticles
    DOI:  https://doi.org/10.1016/j.mtbio.2025.102465
  7. Immunol Res. 2025 Nov 13. 73(1): 164
      In their recent study, Jedlička et al. demonstrate that glutaminase (GLS) activity is indispensable for sustaining human natural killer (NK) cell cytotoxicity, positing it as a key metabolic regulator of effector function. While this work provides a valuable foundation for understanding NK cell immunometabolism, our analysis identifies several critical areas requiring deeper exploration. This letter offers a prospective critique, highlighting the incomplete delineation of the downstream metabolic mechanisms-specifically regarding energy production, biosynthetic precursor synthesis, and redox homeostasis-that link GLS activity to the cytolytic machinery. Furthermore, we question the physiological relevance of these in vitro findings within the nutrient-deprived and competitive tumor microenvironment (TME), where NK cells must exhibit metabolic flexibility. A paramount concern is the translational double-edged sword of GLS inhibition, which may inadvertently suppress anti-tumor immunity. We conclude that future research must employ integrated multi-omics and in vivo models to resolve these complexities, which is essential for harnessing NK cell metabolism without compromising its therapeutic potential.
    Keywords:  GlutaminaseNatural Killer cellsImmunometabolismCytotoxicityGlutaminolysisTumor microenvironment
    DOI:  https://doi.org/10.1007/s12026-025-09724-4
  8. Front Immunol. 2025 ;16 1689790
      Osteosarcoma (OS) is the most common primary malignant bone tumor, predominantly affecting adolescents and young adults. Despite decades of research, survival rates for metastatic or recurrent disease remain dismal, underscoring the urgent need for therapeutic innovation. This malignancy frequently exhibits refractory responses to immunotherapy, a limitation increasingly attributed to dysregulated immunometabolic crosstalk. Growing evidence supports cellular metabolism as a master regulator of both neoplastic progression and immune cell functionality. To meet heightened biosynthetic demands, OS cells undergo metabolic reprogramming, adopting distinct programs divergent from normal counterparts. These changes reshape the tumor microenvironment (TME) into an immunosuppressive milieu, restricting immune cell infiltration and effector activity. Consequently, targeting these immunometabolic pathways offers a promising strategy to overcome therapeutic resistance. Here, we critically analyze the current understanding of OS immunometabolism, systematically delineating OS-specific evidence from extrapolated concepts. We dissect the key metabolic barriers to successful immunotherapy and propose a forward-looking roadmap to guide the development of more effective, biomarker-driven therapeutic strategies.
    Keywords:  immunometabolism; immunotherapy; metabolic reprogramming; osteosarcoma; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2025.1689790
  9. MedComm (2020). 2025 Nov;6(11): e70479
      Stress granules (SGs) are cytoplasmic condensates that regulate mRNA translation and signaling in response to stress. Although SGs have been widely studied in antiviral responses, their function in bacterial infections is not well understood. Here, we demonstrate that SGs promote Mycobacterium tuberculosis (Mtb) pathogenesis by suppressing mitochondrial metabolism and innate immunity. Quantitative proteomics revealed that Mtb-induced SGs sequester mTORC1 and suppress cap-dependent mRNA translation. This leads to decreased expression of proteins necessary for mitochondrial respiration and immune activation in bone marrow-derived macrophages (BMDMs). Disrupting SG assembly restored mTORC1 signaling, enhanced oxidative phosphorylation, and increased the production of antimicrobial mediators, such as reactive oxygen species, nitric oxide, and proinflammatory cytokines. This restricted intracellular Mtb growth in vitro and in vivo. Mechanistically, intracellular ATP depletion triggered by Mtb phagocytosis was sufficient to drive SG formation, linking energy stress to translational repression. Furthermore, SGs captured Ndufa12, a complex I subunit, thereby impairing mitochondrial electron transport and ATP production. These findings identify SGs as key regulators that couple translational arrest to metabolic and immune suppression, enabling Mtb persistence. Targeting SG formation or function could be a host-directed strategy to restore mitochondrial activity and strengthen immune responses against Mtb infection.
    Keywords:  ATP; Mycobacterium tuberculosis; mitochondria; stress granule; tuberculosis
    DOI:  https://doi.org/10.1002/mco2.70479
  10. Cells. 2025 Nov 06. pii: 1743. [Epub ahead of print]14(21):
      Viruses account for the most abundant biological entities in the biosphere and can be either symbiotic or pathogenic. While pathogenic viruses have developed strategies to evade immunity, the host immune system has evolved overlapping and redundant defenses to sense and fight viral infections. Nutrition and metabolic needs sculpt viral-host interactions and determine the course and outcomes of the infection. In this review, we focus on the hexosamine biosynthesis pathway (HBP), a nutrient-sensing pathway that controls immune responses and host-viral interactions. The HBP converges on O-GlcNAcylation, a dynamic post-translational modification of cellular proteins, that emerged as a critical effector of immune cell development, differentiation, and effector functions. We present a broad overview of uncovered O-GlcNAc substrates identified in the context of viral infections and with a functional impact on antiviral immunity and viral restriction, or conversely on exacerbating viral-induced pathologic inflammation or viral oncogenesis. We discuss the clinical implications of these findings, current limitations, and future perspectives to harness this pathway for therapeutic purposes.
    Keywords:  glycosylation; host–pathogen interaction; immunometabolism; infection; inflammation; innate immunity; nutrient sensing; pattern-recognition receptors; post-translational modification; virus
    DOI:  https://doi.org/10.3390/cells14211743
  11. Trends Cell Biol. 2025 Nov 13. pii: S0962-8924(25)00244-2. [Epub ahead of print]
      Cholesterol is an essential lipid component of membrane bilayers that maintains proper cellular function. Macrophages, key innate immune cells, are involved in organ development, tissue repair, defense against infection, and tumor progression. Accumulating evidence indicates that macrophages undergo significant reprogramming of cholesterol metabolism in response to external signals from diverse pathological microenvironments. This review provides a comprehensive overview of the cellular and systemic regulation of cholesterol metabolism homeostasis and examines how cholesterol metabolites regulate macrophage function. It highlights recent advances in targeting cholesterol metabolism for therapeutic purposes in various human diseases, including neurodegenerative diseases, atherosclerosis, bacterial and viral infections, and cancer.
    Keywords:  atherosclerosis; cholesterol metabolism; infection; macrophage; neurodegenerative diseases; tumor
    DOI:  https://doi.org/10.1016/j.tcb.2025.10.003
  12. Cell Mol Immunol. 2025 Nov 14.
      Intracerebral hemorrhage (ICH) causes hematoma formation, leading to PHE, which is associated with leukocyte mobilization and increased inflammation at the site of brain injury. However, the fate of accumulated leukocytes within the hematoma and their impact on PHE expansion remain unknown. We performed single-cell immune profiling of hematoma cells from patients with acute ICH and reported a distinct phenotypic transformation of CD8+ T cells within the hematoma during the first 24 h after onset. In addition to enhanced IFN-γ production and migration capacity, these CD8+ T cells displayed remarkable glycolytic signatures. The metabolic fitness and functional reprogramming of hematomal CD8+ T cells are associated with the transcription factor FOXO1. Single-cell profiling of brain-infiltrating CD8+ T cells within the perihematomal tissues of ICH patients and cell culture assays revealed their capacity to activate microglia via the production of IFN-γ. Furthermore, the removal of hematomal CD8+ T cells reduced neuroinflammation, PHE expansion and neurological deficits in ICH mice. Thus, CD8+ T cells undergo metabolic and functional reprogramming within the hematoma during the acute phase of ICH, which contributes to PHE formation and neurological deterioration.
    Keywords:  CD8+ T cells; Hematoma; Intracerebral hemorrhage; Neuroinflammation; Perihematomal edema
    DOI:  https://doi.org/10.1038/s41423-025-01363-x
  13. Int J Mol Sci. 2025 Oct 28. pii: 10461. [Epub ahead of print]26(21):
      During infection, myeloid cells are subjected to a fast increase in energy demand. Glucose transporter 1 (GLUT1) is a key mediator of glucose metabolism, especially for glycolysis. The present study aimed to investigate GLUT1 expression in monocytes and neutrophils from patients with community-acquired pneumonia (CAP) and to determine the functional role of GLUT1 in the responsiveness during pneumonia evoked in mice by Streptococcus (S.) pneumoniae, the most common causative pathogen in CAP. GLUT1 expression in monocytes and neutrophils of patients and controls was determined by RNA sequencing and flow cytometry analysis. Myeloid cell-specific GLUT1-deficient mice and controls were intranasally infected with S. pneumoniae, after which bacterial loads, lung pathology, and cytokine levels were analyzed. GLUT1 gene expression was upregulated in monocytes from CAP patients in comparison to matched subjects without infection, and protein expression was increased upon ex vivo activation. In neutrophils, GLUT1 mRNA levels were significantly upregulated in CAP patients, but protein levels were not altered. Surprisingly, myeloid-specific GLUT1-deficient mice displayed an unaltered host response during pneumococcal pneumonia. These data suggest that GLUT1 may contribute to immune responses of myeloid cells during CAP, but that its role may be superseded by other mechanisms during pneumococcal pneumonia.
    Keywords:  GLUTs; bacterial infection; experimental pneumonia model; immune response; macrophages; mice; monocytes; neutrophils
    DOI:  https://doi.org/10.3390/ijms262110461
  14. Curr Allergy Asthma Rep. 2025 Nov 11. 25(1): 53
       PURPOSE OF REVIEW: The gut microbiota contributes to host homeostasis through the production of bioactive metabolites that regulate immune function. Some of these microbial metabolites, called short-chain fatty acids (SCFA), have been extensively associated with allergic diseases. However, this review aims to focus on other families of microbial metabolites that are also involved in regulating the immune and inflammatory responses. These include branched SCFA (BCFA), tryptophan and tyrosine (and their derivatives), secondary bile acids (BA), sphingolipids (SL), histamine, polyamines, and odd-chain fatty acid (OCFA)-containing metabolites.
    RECENT FINDINGS: In addition to the canonical SCFA, BCFA are also important regulators of innate and adaptive immunity. Specifically, they appear to participate in the mechanisms underlying allergic resolution and tolerance development. Furthermore, microbial derivatives of tryptophan, such as indole-3-acetic acid and indole-3-propionic acid, have been shown to regulate T helper 17 (Th17) and regulatory T cell populations, thereby reducing the allergic response. Products of the bacterial metabolism of other aromatic amino acids, such as tyrosine, are also associated with pro- and anti-inflammatory properties. Regarding secondary BA, isolithocholic acid has recently emerged as a key inhibitor of the Th17 response. Additionally, SL help maintain epithelial integrity and modulate the inflammatory response by regulating the levels of bioactive lipids, including ceramides and sphingosine-1-phosphate. Lastly, alterations in the bacterial metabolism of polyamines, including spermidine, and OCFA-containing metabolites, including lysophosphatidylcholines (LCP), have also been reported in allergic diseases. The microbiota metabolism modulates the immune response of its host and represents a potential target for the implementation of personalized therapeutic strategies in allergic patients.
    Keywords:  Bile acids; Histamine; Immune system; Metabolomics; Sphingolipids; Tryptophan and tyrosine metabolism
    DOI:  https://doi.org/10.1007/s11882-025-01231-8
  15. Front Immunol. 2025 ;16 1676550
       Background/Introduction: The utility of measuring real-time cellular bioenergetics of peripheral blood mononuclear cells (PBMCs) as biomarkers in disease monitoring, such as the bioenergetic health index, is of emerging interest. However, various experimental factors can impact the accuracy and reproducibility of these measurements.Methods: PBMC bioenergetics were probed in real-time using extracellular flux analysis to identify optimal seeding density and injection protocol. Using a modified protocol, we assessed the extent to which blood processing time and isolation method (SepMate™ vs. EasySep™ Direct) influence PBMC bioenergetics under basal and stimulated conditions. Advanced metabolic control analysis including mitochondrial and glycolytic ATP supply flux, respiratory control ratio, bioenergetic health index, and mitochondrial toxicity index were used to identify and quantify PBMC bioenergetics.
    Results: Measures of metabolic profiling such as mitochondrial respiration, glycolytic activity, ATP supply flux, and respiratory control ratio were significantly diminished in PBMCs due to blood processing delay (48-72 hours) and were influenced by isolation method. Extended blood processing time significantly lowered T cell activation capacity in PBMCs, evidenced by decreased responses of mitochondrial and glycolytic ATP supply to CD3/CD28 activation.
    Discussion/Conclusion: This study demonstrates that key experimental variables including blood processing time and isolation method critically affect the reliability and biological relevance of PBMC metabolic assessments, highlighting the importance of protocol standardisation for accurate bioenergetic biomarker measurements.
    Keywords:  PBMCs; bioenergetics; blood processing time; extracellular flux analysis; glycolysis; metabolic profiling; mitochondria
    DOI:  https://doi.org/10.3389/fimmu.2025.1676550
  16. IBRO Neurosci Rep. 2025 Dec;19 792-800
      Chronic inflammation is central to both multiple sclerosis (MS) and allergic conditions, though their pathological outcomes differ. In MS, inflammation leads to demyelination and neurodegeneration in the central nervous system, while in allergies, it causes localized tissue swelling and irritation. Emerging evidence suggests that heightened immune activity in allergies may influence or exacerbate inflammatory responses in MS, with some researchers proposing shared immunopathological mechanisms between allergic hyperactivity and the autoimmune processes underlying MS. The kynurenine pathway, a key route of tryptophan metabolism, has garnered attention for its role in the pathogenesis of neurodegenerative, psychiatric, vascular, and autoimmune diseases. Its metabolites are known to modulate neuroinflammation and immune responses, particularly through their effects on B and T lymphocytes, which are critical in adaptive immunity and autoimmune pathology. This article explores the influence of the kynurenine pathway on B and T lymphocyte function, aiming to determine its potential to provide deeper insights into immune dysregulation in chronic inflammation diseases. By understanding these interactions, we seek to evaluate the kynurenine pathway as a target for developing more effective therapeutic strategies for chronic inflammations and autoimmune conditions.
    Keywords:  Allergic conditions; B immune cells; Chronic inflammation; Kynurenic pathways; Multiple sclerosis; T immune cells; Tryptophan metabolism
    DOI:  https://doi.org/10.1016/j.ibneur.2025.10.009
  17. Adv Sci (Weinh). 2025 Nov 11. e08957
      Depression is one of the most prevalent neuropsychiatric disorders worldwide, and multiple studies have implicated metabolic dysfunction in its pathophysiology. However, the molecular mechanisms by which metabolic pathways modulate depressive‑like behavior remain largely uncharacterized. Here, this work finds that the CDGSH iron sulfur domain 1 (CISD1), a redox protein localized to the outer mitochondrial membrane, is upregulated in the medial prefrontal cortex after chronic stress. Pharmacological inhibition and genetic knockdown of CISD1 significantly ameliorate depressive-like behavior in mice, and CISD1 knockdown also reverse microglial inflammatory activation. Moreover, this work finds that chronic stress specifically upregulates microglial CISD1 expression, and that conditional knockout of microglial CISD1 alleviates neuroinflammation and depressive‑like behavior in mice. Mechanistically, chronic stress promotes NADH oxidation to generate NAD⁺ by upregulating CISD1 expression. The elevated NAD⁺ functions as a cofactor for glyceraldehyde-3-phosphate dehydrogenase, accelerating glycolysis and promoting inflammatory activation. Pioglitazone exerts antidepressant effects by inhibiting NADH oxidation through a CISD1-dependent pathway in microglia. In conclusion, this study elucidates the role of CISD1 in microglial metabolism, establishing a robust experimental foundation for screening potential antidepressant drugs.
    Keywords:  CDGSH iron sulfur domain 1; depression; medial prefrontal cortex; microglial inflammatory activation; pioglitazone
    DOI:  https://doi.org/10.1002/advs.202508957
  18. mBio. 2025 Nov 10. e0255425
      Viral pathogens employ diverse strategies to antagonize host antiviral innate immune defenses. However, the human-specific nature of viral immune evasion mechanisms remains poorly understood. Here, we report that herpesvirus infection selectively activates the embryonic transcription factor DUX4 in human but not murine cells. DUX4 drives the expression of the phosphate transporter SLC34A2, which plays a critical role in suppressing antiviral innate immunity. Mechanistically, SLC34A2 increases intracellular phosphate levels, thereby suppressing the activity of multiple immune and stress-related kinases, including TBK1. Genetic disruption of DUX4 or SLC34A2 restores innate immune activation and enhances interferon responses. Our findings reveal a previously unrecognized, phosphate-mediated immunosuppressive mechanism and define a human-specific transcriptional circuit exploited by herpesviruses to antagonize innate immunity.IMPORTANCEHerpesviruses are notorious for their ability to evade host immune responses, yet the mechanisms underlying human-specific immune evasion remain poorly understood. This study identifies a previously unrecognized viral immune evasion strategy by which herpesviruses suppress antiviral immunity in human cells but not murine cells. We demonstrate that herpesvirus infection induces the expression of the embryonic transcription factor DUX4, which subsequently activates its downstream target, SLC34A2, a phosphate transporter. DUX4-SLC34A2 activation reprograms infected cells toward an embryonic-like transcriptional profile, creating an environment conducive to viral replication. Importantly, we show that SLC34A2 increases intracellular phosphate levels, thereby suppressing the activity of multiple immune and stress-related kinases, including TBK1. Our findings reveal a previously unrecognized phosphate-mediated regulation of antiviral immunity, providing insights into viral-host interactions and highlighting therapeutic targets for enhancing antiviral defense.
    Keywords:  antiviral innate immunity; herpesvirus; immune evasion; phosphate
    DOI:  https://doi.org/10.1128/mbio.02554-25
  19. Autophagy. 2025 Nov 13.
      Mitochondrial nicotinamide adenine dinucleotide (NAD+) plays a central role in energy metabolism, yet its roles and mechanisms in mitophagy and innate immunity remain poorly understood. In this study, we identify mitochondrial NAD+ depletion that causes mitophagy dysfunction and inflammation. We find that depletion of mitochondrial NAD+ owing to deficiency of the mitochondrial NAD+ transporter SLC25A51 impairs BNIP3-mediated mitophagy. Loss of mitochondrial NAD+ inhibits SIRT3-mediated deacetylation of FOXO3, leading to transcriptional downregulation of BNIP3 and subsequent disruption of MAP1LC3B/LC3B recruitment. Notably, mitochondrial NAD+ depletion promotes mitochondrial DNA (mtDNA) release from mitochondria to the cytosol upon oxidative stress, thereby exacerbating the type I interferon response to free cytosolic mtDNA via activation of the CGAS-STING1 signaling pathway. Our findings reveal a novel mechanistic link among mitochondrial NAD+, mitophagy, and mtDNA-induced inflammation by genetic manipulation of cell lines, highlighting mitochondrial NAD+ as a potential therapeutic target for mitigating sterile inflammation triggered by free cytosolic mtDNA. Thus, the study provides new insights into the crosstalk among mitochondrial homeostasis, inflammation, and innate immunity.
    Keywords:  Cytosolic mtDNA; SLC25A51; inflammation; innate immunity; mitochondrial NAD+; mitophagy
    DOI:  https://doi.org/10.1080/15548627.2025.2589909
  20. Int J Mol Sci. 2025 Oct 31. pii: 10630. [Epub ahead of print]26(21):
      Diabetic retinopathy (DR), a major complication of diabetes, is driven by chronic inflammation in which retinal microglial cells play a central role. The Hippo pathway kinases NDR1/2 regulate macrophage function, but their role in microglia and DR remain unknown. This study investigates the function of the NDR2 kinase in microglial cells under high-glucose (HG) conditions. Using CRISPR-Cas9, we partially knocked out the Ndr2/Stk38l gene in BV-2 mouse microglial cells and analyzed metabolic activity, phagocytosis, migration, and cytokine release. We confirmed NDR2 expression in microglia and observed increased levels under HG, suggesting a role in hyperglycemia-induced stress. Ndr2/Stk38l (hereafter referred to as Ndr2) downregulation impaired mitochondrial respiration and reduced metabolic flexibility, indicating defective stress adaptation. Functionally, microglia with a partial downregulation of Ndr2 displayed reduced phagocytic and migratory capacity-both dependent on cytoskeletal dynamics. Moreover, Ndr2 downregulation altered the secretory profile, elevating pro-inflammatory cytokines (IL-6, TNF, IL-17, IL-12p70) even under normal glucose levels. These findings identify NDR2 protein kinase as a key regulator of microglial metabolism and inflammatory behavior under diabetic conditions. By modulating immune and metabolic responses, NDR2 may contribute to the neuroinflammatory processes underlying DR. Targeting NDR2 function in microglia may offer novel therapeutic strategies to mitigate retinal inflammation and progression of DR.
    Keywords:  Ndr2/Stk38l gene; Nuclear Dbf2-Related (NDR) kinases; diabetic retinopathy; high-glucose; inflammation; metabolism; microglia; retina
    DOI:  https://doi.org/10.3390/ijms262110630
  21. Curr Res Microb Sci. 2025 ;9 100496
      Short-chain fatty acids (SCFAs) are crucial microbial metabolites that mediate host-microbiota interactions, regulate immune responses, and maintain gut homeostasis. While most studies focus on SCFA production by obligate anaerobes, recent evidence highlights Lactobacillus spp. as potential SCFA-producing microorganisms that remain understudied in terms of SCFA-based health and food-related effects. This research review compiles what is currently known about species- and strain-specific biosynthetic capabilities of Lactobacillus for SCFA production, particularly acetate, and lactate, which, while produced by Lactobacillus, is not classified as a SCFA but plays similar metabolic roles (e.g., activation of G-protein-coupled receptors, inhibition of histone deacetylases, and immune cell metabolism). We additionally assess new synthetic biology and metabolic engineering approaches to improving SCFA yield in Lactobacillus, including gene circuit design, CRISPR editing, and co-culture optimization. Importantly, we discuss translational opportunities not only in inflammatory, metabolic, and neuroimmune diseases but also in the development of functional foods, synbiotics, and nutraceutical applications. Finally, we highlight key challenges-strain variability, delivery strategies, and regulatory oversight-that preclude both clinical and food system translation. By integrating perspectives from microbiology, immunology, food science, and bioengineering, this review provides a broad framework for the rational design of SCFA-producing Lactobacillus strains as next-generation probiotics and food-grade biotherapeutics.
    Keywords:  Gut microbiome; Lactobacillus; Probiotics; Short-chain fatty acids (SCFAs); Synthetic biology
    DOI:  https://doi.org/10.1016/j.crmicr.2025.100496
  22. Curr Allergy Asthma Rep. 2025 Nov 10. 25(1): 51
       PURPOSE OF THE REVIEW: The innate immune system plays a critical role in mediating many of the physiological consequences of high-fat diet consumption. Dietary lipids, and specifically saturated fatty acids like palmitate and stearate, directly activate innate immune cells and alter the composition of the gut microbiome. Moreover, long-term high-fat diet feeding can induce chronic inflammation, adipose expansion, and the development of obesity. High-fat diet consumption and obesity also worsen the risk for chronic diseases like asthma.
    RECENT FINDINGS: It is well known that high-fat diet feeding activates innate immune cells and alters the gut microbiome. However, emerging research provides new insight into the mechanisms by which high-fat diet feeding and obesity affect innate immunity and further disease development. These emerging mechanisms include the induction of lipid-associated macrophages (LAMs), innate immune memory, and innate-adaptive crosstalk leading to T cell exhaustion and granzyme K production. These novel mechanisms help us better understand the effect of high-fat diets on innate immunity, and future studies in these areas may help us better identify new therapeutic strategies for managing obesity and asthma.
    Keywords:  Allergic disease; Immunometabolism; Metabolic disease; Trained innate immunity; Weight loss
    DOI:  https://doi.org/10.1007/s11882-025-01232-7
  23. Sci Immunol. 2025 Nov 14. 10(113): eadz5181
      Pancreatic islet-resident macrophages (IRMs) display an activated phenotype and contribute to islet development and remodeling, yet their origin, heterogeneity, and functional roles remain poorly understood. Using complementary fate-mapping systems, we show that, in adult mice, around half of IRMs originate from circulating monocytes and undergo minimal turnover. Integrated multiple single-cell RNA sequencing analyses of mouse and human islets identified four major IRM cell states that collectively reveal their inflammatory and metabolic activation. Among these, a transcriptional program driven by the cystine-glutamate antiporter SLC7A11 and enriched in CD9high IRMs was associated with enhanced antioxidant defense, mitochondrial activity, and iron-lipid metabolic pathways. We found that Slc7a11-expressing IRMs preserve β cell redox homeostasis and insulin secretion, both at baseline and under stress. These findings position IRMs as specialized immune sentinels in the endocrine pancreas and identify SLC7A11 as a key macrophage-intrinsic safeguard against oxidative stress, with broad implications for islet resilience and metabolic health.
    DOI:  https://doi.org/10.1126/sciimmunol.adz5181
  24. J Clin Invest. 2025 Nov 11. pii: e198387. [Epub ahead of print]
      Familial partial lipodystrophy 2 (FPLD2) is a rare disease characterized by adipose tissue loss and redistribution, and metabolic dysfunction. FPLD2 is caused by pathogenic variants in the LMNA gene, encoding nuclear lamins A/C, structural proteins that control nuclear function and gene expression. However, the mechanisms driving adipocyte loss in FPLD2 remain poorly defined. In this study, we recruited eight families with developing or established FPLD2 and performed clinical, histological, and transcriptomic analyses of subcutaneous adipose tissue biopsies. Bulk and single-nuclei RNA-sequencing revealed suppression of lipid metabolism and mitochondrial pathways, alongside increased inflammation. These signatures were mirrored in tamoxifen-inducible adipocyte-specific Lmna knockout mice, in which lamin A/C-deficient adipocytes shrank and disappeared. Lmna-deficient fibroblasts shared similar gene expression changes, linked to altered chromatin accessibility, underscoring lamin A/C's potential regulatory role in lipid metabolism and inflammatory programs. By directly comparing atrophic and hypertrophic adipose depots in FPLD2, and integrating human, mouse, and in vitro models, this study provides new insights into disease progression and potential therapeutic targets.
    Keywords:  Adipose tissue; Bioinformatics; Clinical Research; Genetic diseases; Metabolism
    DOI:  https://doi.org/10.1172/JCI198387
  25. Front Immunol. 2025 ;16 1626581
       Introduction: Immunotherapy efficacy in gastric cancer (GC) is often constrained by the tumor microenvironment (TME), which is profoundly influenced by aberrant metabolism. Asparagine, an amino acid critical for neoplastic proliferation, also modulates CD8+ T cell metabolic programming. We investigated the impact of targeting asparagine on the GC immune microenvironment and its potential to synergize with anti-PD-L1 therapy.
    Methods: The therapeutic efficacy of asparagine targeting was evaluated in GC tumor models. CD8+ T cell populations within the TME were analyzed by flow cytometry, while cytokine and chemokine levels (IFN-γ, GZMB, CXCL9, CXCL10) were quantified by ELISA. The effects on CD8+ T cell activation and antitumor function were assessed in vitro and in vivo. Synergistic efficacy with anti-PD-L1 therapy was evaluated in GC models, and the dependency on CD8+ T cells was confirmed via antibody-mediated depletion experiments.
    Results: Targeting asparagine inhibited GC growth in vitro and in vivo, implicating immune system involvement. Mechanistically, asparagine targeting significantly increased the proportion of CD8+ T cells within the TME and upregulated the expression of IFN-γ, GZMB, CXCL9, and CXCL10. Furthermore, combining asparagine targeting with anti-PD-L1 therapy produced synergistic antitumor activity. This combined therapeutic effect was significantly attenuated by the depletion of CD8+ T cells.
    Discussion: Our findings indicate that targeting asparagine promotes CD8+ T cell activation and infiltration, thereby remodeling the GC immune microenvironment to enhance host antitumor immunity. The combination of asparagine targeting with anti-PD-L1 therapy elicits potent, synergistic antitumor effects that are demonstrably dependent on CD8+ T cells. This study provides a strong rationale for targeting asparagine metabolism as a novel strategy to improve immunotherapeutic outcomes in GC.
    Keywords:  CD8 T cell; TME (tumor microenvironment); asparagine; gastric cancer; immunotherapy; metabolism
    DOI:  https://doi.org/10.3389/fimmu.2025.1626581
  26. Biochem Biophys Res Commun. 2025 Oct 30. pii: S0006-291X(25)01605-5. [Epub ahead of print]791 152889
      Dexamethasone (DEX) is a widely used immunosuppressant that predisposes hosts to opportunistic infections like Pneumocystis pneumonia (PCP). However, the precise immunological and metabolic mechanisms by which DEX alters pulmonary immunity against Pneumocystis remain poorly understood. Using single-cell RNA sequencing on lung tissues of PCP model of control and DEX-induced immunocompromised mouse (DEX-PCP), we found that DEX related immunosuppression reshaped the pulmonary cellular landscape. It increased neutrophil and monocyte proportions while diminishing lymphocytes. Notably, neutrophils, despite being expanded, their pro-inflammatory and antibacterial capabilities were impaired, including reduced ROS production and phagocytic pathways. Metabolic analysis revealed a specific and profound suppression of fatty acid oxidation (FAO) in DEX-PCP neutrophils. Further flow cytometry, RT-qPCR, bulk RNA-seq and metabolomics assays verified the down-regulation of the FAO pathway and key antibacterial mediators. In conclusion, our study demonstrates that DEX-induced immunosuppression in PCP subverts neutrophil function by reprogramming their metabolic state, specifically through the impairment of FAO.
    Keywords:  Dexamethasone; Fatty acid oxidation; Neutrophil; Pneumocystis pneumonia
    DOI:  https://doi.org/10.1016/j.bbrc.2025.152889
  27. Phytomedicine. 2025 Nov 01. pii: S0944-7113(25)01143-2. [Epub ahead of print]149 157506
       BACKGROUND: Panax notoginseng saponin (PNS) has shown potent activities in treating patients with atherosclerosis (AS), whereas its immunometabolic mechanism remained unknown.
    OBJECTIVES: To elucidate the characteristics of metabolomics of AS plaque and identify immunometabolic mechanisms of PNS in treating AS.
    METHODS: PNS components were characterized using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MSE). Spatial Metabolomics was performed to reveal characteristics of plaque from atherosclerosis patients. Then we verified different glycolysis and sphingolipid metabolites between chronic coronary disease (CCD) patients and health control (HC). In vivo and in vitro experiments were performed to study the relationship among hypoxia-inducible factor-1 α (Hif-1α), glycolysis, and macrophage polarization, as well as the protective role and underlying mechanism of PNS in AS.
    RESULTS: Among 8058 metabolites, 117 metabolites were greatly downregulated and 355 metabolites were remarkably upregulated in the plaque area. Sphingolipid metabolism ranked the top according to KEGG analysis, among which sphingosine-1-phosphate (S1P) and specifically sphingomyelin (SPH) were significantly reduced in CCD patients. Overexpression of Hif-1α could induce macrophage M1 polarization, enhance glycolysis, promote excessive UDP-glucose ceramide glucosyltransferase (UGCG) production, and reduce S1P, resulting in a proinflammatory response. Chemical characterization of PNS verified the presence of the principal saponins (R1, Rg1, Rb1, Rd, Re), which subsequently was shown to act as a novel Hif-1α inhibitor, exerting its anti-atherosclerotic effects through multiple pathways, specifically, downregulating key glycolytic regulators (PFKFB3, GLUT1, HK2) and suppressing downstream glycolysis; promoting the expression of MRC1/iNOS to inhibit M1 macrophage polarization; upregulating S1P to modulate sphingolipid metabolism, thereby alleviating AS.
    CONCLUSION: These findings emphasize the anti-AS effects of PNS through a novel immunometabolic mechanism, particularly its role as a Hif-1α inhibitor that disrupts such pathways driving AS progression.
    Keywords:  Atherosclerosis; Glycolysis; Macrophage polarization; Panax notoginseng saponin; Sphingolipid metabolism pathway
    DOI:  https://doi.org/10.1016/j.phymed.2025.157506
  28. Immunometabolism (Cobham). 2025 Oct;7(4): e00074
      Most chronic diseases including coronary heart disease, obesity, diabetes, cancer, and multiple neurodegenerative diseases are driven by dysregulated lipid metabolism. In fact, many common drugs taken by millions including aspirin, statins, fibrates, and others improve health by reorganizing systemic lipid metabolism. Although we have a wealth of information on the enzymes and pathways maintaining lipid metabolic homeostasis in our human cells, there is much less known in regard to how our gut microbiome may coordinate with the host to control systemic lipid metabolism. With advances in untargeted metabolomics, there is a rapidly expanding list of gut microbe-derived lipid metabolites with unannotated function. Many of these bacterial lipids can be assimilated into host lipids and alter host lipid metabolic processes. Here, we discuss how gut microbe-derived lipids may be further metabolized by the host through metaorganismal metabolic pathways. We also discuss the untapped therapeutic potential for targeting metaorganismal lipid metabolism for the improvement of human health.
    Keywords:  lipid; metabolism; microbiome
    DOI:  https://doi.org/10.1097/IN9.0000000000000074
  29. Science. 2025 Nov 13. 390(6774): 686
      Nucleotide-centric defense systems reveal a core principle in bacterial antiviral immunity.
    DOI:  https://doi.org/10.1126/science.aec9672
  30. J Exp Clin Cancer Res. 2025 Nov 14. 44(1): 306
       BACKGROUND: Metabolic reprogramming, particularly upregulated de novo pyrimidine biosynthesis, drives cancer progression and immune evasion. Dihydroorotate dehydrogenase (DHODH), a key enzyme in this pathway, is a promising therapeutic target, but its inhibitors often face resistance in immune-refractory melanoma, linked to low basal stimulator of interferon genes (STING) expression.
    METHODS: To overcome this limitation, we designed H62, a tumor-selective prodrug conjugating the DHODH inhibitor EA6 with the STING agonist MSA-2 via a cathepsin B-cleavable linker. Mechanistic studies evaluated mitochondrial disruption, pyroptosis (caspase-3/GSDME), and STING-mediated interferon signaling, alongside natural killer (NK) cell recruitment. Efficacy was tested in multiple melanoma models, including standard and neoadjuvant settings.
    RESULTS: H62 synergistically induced mitochondrial dysfunction and pyroptosis while activating STING/type I interferon responses, enhancing NK cell cytotoxicity. In melanoma models, it significantly suppressed tumor growth, reduced postoperative recurrence, and improved survival.
    CONCLUSIONS: This dual-targeting strategy overcomes DHODH inhibitor resistance by coupling metabolic interference with innate immune activation, offering translational potential for melanoma and other treatment-resistant cancers.
    Keywords:  DHODH inhibitor resistance; Immunometabolism; NK cell; Pyroptosis; STING pathway
    DOI:  https://doi.org/10.1186/s13046-025-03566-6
  31. Microbiol Spectr. 2025 Nov 11. e0154625
      Salmonella Enteritidis infection has caused substantial economic losses in the poultry industry. Traditional antibiotic treatments have led to issues, such as drug-resistant bacteria and antibiotic residues, which pose significant threats to human and animal health, as well as food and environmental safety. Therefore, establishing new, effective prevention and control methods is of paramount importance. In this study, we utilized gas chromatography-mass spectrometry (GC-MS) metabolomics to analyze the metabolomic profiles of chickens infected with varying concentrations of Salmonella Enteritidis. Significant differences in the metabolomes were observed, with citrulline identified as a candidate biomarker, showing increased levels corresponding to higher infection doses. Exogenous addition of citrulline was found to upregulate the expression of the inducible nitric oxide synthase (iNOS) gene in the urea cycle of chicken HD11 macrophages, leading to increased nitric oxide (NO) levels and enhanced phagocytosis of Salmonella Enteritidis by HD11 cells. Furthermore, in vivo challenge experiments demonstrated that exogenous citrulline improved the ability of chickens to clear Salmonella Enteritidis and increased their survival rate post-infection. Importantly, this effect could be attenuated by the iNOS inhibitor 1400W. Thus, our study presents a novel strategy for combating bacterial infections through metabolic modulation.
    IMPORTANCE: Chickens respond to Salmonella infection by adjusting the metabolic state of their bodies. Citrulline can enhance the phagocytic ability of phagocytes by strengthening the urea cycle. In vitro clinical trials have revealed that citrulline can increase the survival rate of chickens after Salmonella infection.
    Keywords:  Salmonella Enteritidis; chicken; citrulline; metabolomics; nitric oxide
    DOI:  https://doi.org/10.1128/spectrum.01546-25
  32. Virulence. 2025 Nov 10. 2585620
      
    Keywords:  Brucella; brucella virulence factors; immune evasion; metabolic reprogramming; type I interferon; unfolded protein response
    DOI:  https://doi.org/10.1080/21505594.2025.2585620
  33. Mol Biomed. 2025 Nov 10. 6(1): 105
      Traditional antiviral strategies primarily rely on vaccines and virus protein-targeting drugs, which adopt a virus-targeting approach. However, the rapid mutation of viruses often leads to vaccine failure and drug resistance, highlighting the limitations of these conventional methods. Consequently, the development of novel broad-spectrum, host-targeting antiviral strategies has become a major research focus. Itaconate, an endogenous immunomodulatory metabolite, inhibits viral replication via post-translational modifications; however, its mechanism in suppressing viral endocytosis remains unclear. This study demonstrates that itaconate inhibits viral endocytosis by covalently modifying the Cys128 site of the adaptor-related protein complex 1 gamma 1 subunit (AP1G1), thereby providing a new target for host-directed antiviral drug development. It was found that itaconate binds to AP1G1 at Cys128, impairing its interaction with clathrin, which inhibits clathrin-mediated viral particle uptake and reduces cellular susceptibility to infection (i.e., the likelihood of cells being infected by viruses and undergoing infection). Furthermore, the natural product Licochalcone B was identified as targeting the same site as itaconate. In both BEAS-2B cell models and mouse infection models, Licochalcone B reduced pulmonary viral loads by over 95%. This study is the first to propose and validate the feasibility of inhibiting broad-spectrum viral infection by targeting AP1G1, elucidating a novel molecular mechanism of itaconate-mediated regulation, offering a new target for broad-spectrum antiviral drug development, and identifying Licochalcone B as a promising broad-spectrum antiviral agent.
    Keywords:  AP1G1; Clathrin; Itaconate; Post-translational modification; Virus
    DOI:  https://doi.org/10.1186/s43556-025-00348-6
  34. Nat Commun. 2025 Nov 13. 16(1): 9992
      Ferroptosis is a type of iron- and lipid peroxidation-dependent programmed cell death that is involved in various diseases. Some pathogens manipulate host ferroptosis for pathogenesis; however, the potential mechanisms of action remain unclear. Pseudomonas aeruginosa is an opportunistic pathogen that relies on iron for its virulence, biofilm formation, and survival. Here, we report that P. aeruginosa employs the quorum-sensing metabolite, Pseudomonas quinolone signal (PQS), to induce ferroptosis in macrophages through a carnosine-N-methyltransferase (CNMT)-transferrin receptor 1 (TFR1) methylation pathway. Specifically, PQS promotes iron-dependent lipid peroxidation to induce ferroptosis in macrophages. Using high-resolution mass spectrometry-based cellular thermal shift assay (MS-CETSA)/thermal proteome profiling, we identify CNMT as the direct intracellular receptor of PQS in macrophages. Mechanistically, PQS binding increases the histidine methyltransferase (His MTase) activity of CNMT, catalysing methylation of TFR1 at His35. This methylation increases TFR1 protein production, resulting in amplified iron acquisition for ferroptosis. Crucially, the PQS-CNMT-TFR1 axis is distinct from canonical bacterial pathogens that exploit host cell death pathways, revealing the unique strategy of P. aeruginosa to exploit host epigenetic machinery.
    DOI:  https://doi.org/10.1038/s41467-025-65142-y
  35. JCI Insight. 2025 Nov 10. pii: e197169. [Epub ahead of print]10(21):
      Prolonged and dysregulated neutrophilic inflammation causes tissue damage in chronic inflammatory diseases, including antibody-mediated glomerulonephritis (AGN). An increase in glycolysis, supported by enhanced glucose uptake, is a hallmark of hyperneutrophilic inflammation. Neutrophils upregulate glucose transporter 1-mediated (Glut1-mediated) glucose incorporation for renal antimicrobial activities. However, little is known about the role of neutrophil-specific Glut1 function in the pathogenesis of AGN. Using a well-vetted mouse model of AGN, we show that neutrophils upregulate Glut1 expression and function in the nephritic kidney. We demonstrate that Glut1 function in the hematopoietic cells during the early stage of the disease is necessary for kidney pathology. Most importantly, neutrophil-intrinsic Glut1 function is critical for AGN. While neutrophil-specific Glut1 ablation diminished the expression of tissue-damaging effector molecules in both the early and late stages, renal cytokines' and chemokines' production were compromised only in the late stage of the disease. Consequently, Glut1 inhibitor treatment ameliorated renal pathology in AGN mice. These data identify a Glut1-driven inflammatory circuit in neutrophils, which is amenable to therapeutic targeting in AGN.
    Keywords:  Immunology; Inflammation; Innate immunity; Nephrology; Neutrophils
    DOI:  https://doi.org/10.1172/jci.insight.197169
  36. J Biol Chem. 2025 Nov 07. pii: S0021-9258(25)02777-2. [Epub ahead of print] 110925
      Cholinergic adipose macrophages (ChAMs) have recently been shown to regulate the acute thermogenic response in subcutaneous white adipose tissue, yet their transcriptomic dynamics are poorly understood, and little is known about their origins or identity. Using single-cell RNA sequencing (scRNAseq), we profiled ChAT-eGFP+ cells (expressing choline acetyltransferase) from subcutaneous white adipose tissue of mice housed at thermoneutrality or after acute cold exposure. We identified twelve distinct clusters of ChAT-expressing cells, predominated by hematopoietic cell types. Specifically, ChAMs exhibited increased proportions and Chat expression after acute cold. Widespread differential gene expression was induced in ChAMs after cold compared to thermoneutrality, with cold-enriched pathways in immune signaling, chemotaxis, and metabolism. Several ChAM subsets were uncovered that resembled previously reported adipose macrophage subpopulations. ChAMs were predicted to have mixed origins, derived from adult bone marrow and embryonically. These findings provide a high granularity assessment of cholinergic immune cells in fat, and we highlight the transcriptomic plasticity and mixed origins of ChAMs, suggesting their therapeutic potential for metabolic diseases.
    Keywords:  acetylcholine; adipose tissue; macrophage; single-cell RNA-seq; transcriptomics
    DOI:  https://doi.org/10.1016/j.jbc.2025.110925