bims-bac4me Biomed News
on Microbiome and trained immunity
Issue of 2023‒10‒15
39 papers selected by
Chun-Chi Chang, University Hospital Zurich



  1. Front Cell Infect Microbiol. 2023 ;13 1253037
      Lung epithelial cells represent the first line of host defence against foreign inhaled components, including respiratory pathogens. Their responses to these exposures may direct subsequent immune activation to these pathogens. The epithelial response to mycobacterial infections is not well characterized and may provide clues to why some mycobacterial infections are cleared, while others are persistent and pathogenic. We have utilized an air-liquid interface model of human primary bronchial epithelial cells (ALI-PBEC) to investigate the epithelial response to infection with a variety of mycobacteria: Mycobacterium tuberculosis (Mtb), M. bovis (BCG), M. avium, and M. smegmatis. Airway epithelial cells were found to be infected by all four species, albeit at low frequencies. The proportion of infected epithelial cells was lowest for Mtb and highest for M. avium. Differential gene expression analysis revealed a common epithelial host response to mycobacteria, including upregulation of BIRC3, S100A8 and DEFB4, and downregulation of BPIFB1 at 48 h post infection. Apical secretions contained predominantly pro-inflammatory cytokines, while basal secretions contained tissue growth factors and chemokines. Finally, we show that neutrophils were attracted to both apical and basal secretions of infected ALI-PBEC. Neutrophils were attracted in high numbers to apical secretions from PBEC infected with all mycobacteria, with the exception of secretions from M. avium-infected ALI-PBEC. Taken together, our results show that airway epithelial cells are differentially infected by mycobacteria, and react rapidly by upregulation of antimicrobials, and increased secretion of inflammatory cytokines and chemokines which directly attract neutrophils. Thus, the airway epithelium may be an important immunological component in controlling and regulating mycobacterial infections.
    Keywords:  air-liquid interface (ALI) 3D in vitro model; airway epithelium; host-pathogen interaction; non-tuberculous mycobacteria; tuberculosis
    DOI:  https://doi.org/10.3389/fcimb.2023.1253037
  2. mSystems. 2023 Oct 12. e0059323
      Chronic polymicrobial infections (cPMIs) harbor complex bacterial communities with diverse metabolic capacities, leading to competitive and cooperative interactions. Although the microbes present in cPMIs have been established through culture-dependent and culture-independent methods, the key functions that drive different cPMIs and the metabolic activities of these complex communities remain unknown. To address this knowledge gap, we analyzed 102 published metatranscriptomes collected from cystic fibrosis (CF) sputum and chronic wound infections (CW) to identify key bacterial members and functions in cPMIs. Community composition analysis identified a high prevalence of pathogens, particularly Staphylococcus and Pseudomonas, and anaerobic members of the microbiota, including Porphyromonas, Anaerococcus, and Prevotella. Functional profiling with HUMANn3 and SAMSA2 revealed that while functions involved in bacterial competition, oxidative stress response, and virulence were conserved across both chronic infection types, >40% of the functions were differentially expressed. Higher expression of antibiotic resistance and biofilm functions was observed in CF, while tissue-destructive enzymes and oxidative stress response functions were highly expressed in CW samples. Of note, strict anaerobes had negative correlations with traditional pathogens in both CW and CF samples, and they significantly contributed to the expression of these functions. Additionally, we show that microbial communities have unique expression patterns, and distinct organisms fulfill the expression of key functions in each site, indicating that the infection environment strongly influences bacterial physiology and that community structure influences function. Collectively, our findings indicate that community composition and function should guide treatment strategies for cPMIs. IMPORTANCE The microbial diversity in polymicrobial infections (PMIs) allows for community members to establish interactions with one another, which can result in enhanced disease outcomes such as increased antibiotic tolerance and chronicity. Chronic PMIs result in large burdens on health systems, as they affect a significant proportion of the population and are expensive and difficult to treat. However, investigations into physiology of microbial communities in actual human infection sites are lacking. Here, we highlight that the predominant functions in chronic PMIs differ, and anaerobes, often described as bystanders, may be significant in the progression of chronic infections. Determining the community structure and functions in PMIs is a critical step toward understanding the molecular mechanisms that increase the virulence potential of the microbial community in these environments.
    Keywords:  chronic wounds; cystic fibrosis; human infection; microbial community functions; transcriptomics
    DOI:  https://doi.org/10.1128/msystems.00593-23
  3. Clin Dermatol. 2023 Oct 08. pii: S0738-081X(23)00165-7. [Epub ahead of print]
      Emerging evidence highlights the interconnection of the gut-skin microbiota in disease pathogenesis, progression, and as a potential therapeutic target for the management of inflammatory-driven cutaneous diseases. Although not fully understood, recent research has indicated that commensal microbiota and the interaction of the gut-skin axis play an important role in maintaining the skin homeostasis. Dysbiosis and disruption of skin-gut microbiome may lead to impaired skin barrier function thus triggering downstream inflammatory responses involved in the development of inflammatory skin disorders, especially in atopic dermatitis, psoriasis, and hidradenitis suppurativa. Moreover, skin microbiome might also serve as adjunctive therapeutic modalities for treatment. Herein, we review the latest reports on the interrelationship between microbial dysbiosis and inflammatory cutaneous diseases as well as emerging microbiome-directed therapeutics in atopic dermatitis, psoriasis, and hidradenitis suppurativa.
    Keywords:  Skin microbiome; atopic dermatitis; gut microbiome; gut-skin axis; hidradenitis suppurativa; prebiotics; probiotic; psoriasis
    DOI:  https://doi.org/10.1016/j.clindermatol.2023.09.019
  4. Mol Cell Biol. 2023 ;43(10): 531-546
      During the inflammatory response, macrophage phenotypes can be broadly classified as pro-inflammatory/classically activated "M1", or pro-resolving/alternatively "M2" macrophages. Although the classification of macrophages is general and assumes there are distinct phenotypes, in reality macrophages exist across a spectrum and must transform from a pro-inflammatory state to a proresolving state following an inflammatory insult. To adapt to changing metabolic needs of the cell, mitochondria undergo fusion and fission, which have important implications for cell fate and function. We hypothesized that mitochondrial fission and fusion directly contribute to macrophage function during the pro-inflammatory and proresolving phases. In the present study, we find that mitochondrial length directly contributes to macrophage phenotype, primarily during the transition from a pro-inflammatory to a proresolving state. Phenocopying the elongated mitochondrial network (by disabling the fission machinery using siRNA) leads to a baseline reduction in the inflammatory marker IL-1β, but a normal inflammatory response to LPS, similar to control macrophages. In contrast, in macrophages with a phenocopied fragmented phenotype (by disabling the fusion machinery using siRNA) there is a heightened inflammatory response to LPS and increased signaling through the ATF4/c-Jun transcriptional axis compared to control macrophages. Importantly, macrophages with a fragmented mitochondrial phenotype show increased expression of proresolving mediator arginase 1 and increased phagocytic capacity. Promoting mitochondrial fragmentation caused an increase in cellular lactate, and an increase in histone lactylation which caused an increase in arginase 1 expression. These studies demonstrate that a fragmented mitochondrial phenotype is critical for the proresolving response in macrophages and specifically drive epigenetic changes via lactylation of histones following an inflammatory insult.
    Keywords:  fission; fusion; histone lactylation; inflammation resolution; macrophages; mitochondrial metabolism
    DOI:  https://doi.org/10.1080/10985549.2023.2253131
  5. Gut Microbes. 2023 12;15(2): 2267185
      Wang K. et al. introduced the concept of Microbial-Host isozymes (MHIs) and highlighted their role in mediating microbiota-host interactions. They identified bacterial-derived DPP4 as an isoenzyme affecting glucose tolerance and showed that host DPP4 inhibitors may not effectively target bacterial DPP4. They developed an MHI screen system, identifying 71 MHIs in healthy gut microbiota. Among them, DPP4 isozymes degrade GLP-1, explaining variable responses to sitagliptin. This breakthrough opens new avenues for metabolic disorder treatment. However, the complex nature of gut symbiotic bacteria requires further research to understand MHI mechanisms, regulatory roles, and interactions with the host. Precise interventions in gut microbiota offer personalized approaches to metabolic diseases.
    Keywords:  Microbial-Host isozymes; metabolic diseases
    DOI:  https://doi.org/10.1080/19490976.2023.2267185
  6. Front Immunol. 2023 ;14 1230772
      Macrophages play a critical role in the inflammatory response and tumor development. Macrophages are primarily divided into pro-inflammatory M1-like and anti-inflammatory M2-like macrophages based on their activation status and functions. In vitro macrophage models could be derived from mouse bone marrow cells stimulated with two types of differentiation factors: GM-CSF (GM-BMDMs) and M-CSF (M-BMDMs), to represent M1- and M2-like macrophages, respectively. Since macrophage differentiation requires coordinated metabolic reprogramming and transcriptional rewiring in order to fulfill their distinct roles, we combined both transcriptome and metabolome analysis, coupled with experimental validation, to gain insight into the metabolic status of GM- and M-BMDMs. The data revealed higher levels of the tricarboxylic acid cycle (TCA cycle), oxidative phosphorylation (OXPHOS), fatty acid oxidation (FAO), and urea and ornithine production from arginine in GM-BMDMs, and a preference for glycolysis, fatty acid storage, bile acid metabolism, and citrulline and nitric oxide (NO) production from arginine in M-BMDMs. Correlation analysis with the proteomic data showed high consistency in the mRNA and protein levels of metabolic genes. Similar results were also obtained when compared to RNA-seq data of human monocyte derived macrophages from the GEO database. Furthermore, canonical macrophage functions such as inflammatory response and phagocytosis were tightly associated with the representative metabolic pathways. In the current study, we identified the core metabolites, metabolic genes, and functional terms of the two distinct mouse macrophage populations. We also distinguished the metabolic influences of the differentiation factors GM-CSF and M-CSF, and wish to provide valuable information for in vitro macrophage studies.
    Keywords:  GM-CSF; M-CSF; immunometabolism; macrophage differentiation; metabolome; transcriptome
    DOI:  https://doi.org/10.3389/fimmu.2023.1230772
  7. Front Cell Infect Microbiol. 2023 ;13 1242702
      While Staphylococcus aureus (S. aureus) bacteria are part of the human commensal flora, opportunistic invasion following breach of the epithelial layers can lead to a wide array of infection syndromes at both local and distant sites. Despite ubiquitous exposure from early infancy, the life-long risk of opportunistic infection is facilitated by a broad repertoire of S. aureus virulence proteins. These proteins play a key role in inhibiting development of a long-term protective immune response by mechanisms ranging from dysregulation of the complement cascade to the disruption of leukocyte migration. In this review we describe the recent progress made in dissecting S. aureus immune evasion, focusing on the role of the superantigen, staphylococcal protein A (SpA). Evasion of the normal human immune response drives the ability of S. aureus to cause infection, often recurrently, and is also thought to be a major hindrance in the development of effective vaccination strategies. Understanding the role of S. aureus virulence protein and determining methods overcoming or subverting these mechanisms could lead to much-needed breakthroughs in vaccine and monoclonal antibody development.
    Keywords:  B cells; Protein A; Staphylococcus aureus; immune evasion; super antigen; vaccine development
    DOI:  https://doi.org/10.3389/fcimb.2023.1242702
  8. Nutrients. 2023 Oct 04. pii: 4256. [Epub ahead of print]15(19):
      Acute lung injury (ALI) causes lung inflammation and edema as well as resulting in gut microbiota disorder. Probiotics, however, can improve the gut microbiota composition and modulate its immune response, playing an important role in ALI pathogenesis. Therefore, our study aims to investigate the effect of Lactobacillus reuteri on Lipopolysaccharide (LPS)-induced ALI in mice and to probe the mechanism of its synergistic modulatory effect on the lungs and intestines. We assessed the therapeutic effects of L. reuteri in the ALI mouse model by histopathology, alveolar lavage fluid and serum inflammatory factor analysis and explored microbiome and transcriptome alterations. L. reuteri intervention effectively attenuated lung tissue injury and significantly reduced the LPS-induced inflammatory response and macrophage and neutrophil infiltration. Additionally, L. reuteri improved the intestinal barrier function and remodeled the disordered microbiota. In conclusion, our study showed that L. reuteri attenuated the inflammatory response, ameliorated the pulmonary edema, repaired the intestinal barrier, and remodeled the gut microbiota in ALI mice. This study provides new perspectives on the clinical treatment of ALI.
    Keywords:  Lactobacillus reuteri; acute lung injury; gut microbiota; inflammation
    DOI:  https://doi.org/10.3390/nu15194256
  9. Nat Commun. 2023 Oct 13. 14(1): 6454
      Metabolic reprogramming is a hallmark of the immune cells in response to inflammatory stimuli. This metabolic process involves a switch from oxidative phosphorylation (OXPHOS) to glycolysis or alterations in other metabolic pathways. However, most of the experimental findings have been acquired in murine immune cells, and little is known about the metabolic reprogramming of human microglia. In this study, we investigate the transcriptomic, proteomic, and metabolic profiles of mouse and iPSC-derived human microglia challenged with the TLR4 agonist LPS. We demonstrate that both species display a metabolic shift and an overall increased glycolytic gene signature in response to LPS treatment. The metabolic reprogramming is characterized by the upregulation of hexokinases in mouse microglia and phosphofructokinases in human microglia. This study provides a direct comparison of metabolism between mouse and human microglia, highlighting the species-specific pathways involved in immunometabolism and the importance of considering these differences in translational research.
    DOI:  https://doi.org/10.1038/s41467-023-42096-7
  10. EMBO J. 2023 Oct 09. e114086
      The immune response is an energy-demanding process that must be coordinated with systemic metabolic changes redirecting nutrients from stores to the immune system. Although this interplay is fundamental for the function of the immune system, the underlying mechanisms remain elusive. Our data show that the pro-inflammatory polarization of Drosophila macrophages is coupled to the production of the insulin antagonist ImpL2 through the activity of the transcription factor HIF1α. ImpL2 production, reflecting nutritional demands of activated macrophages, subsequently impairs insulin signaling in the fat body, thereby triggering FOXO-driven mobilization of lipoproteins. This metabolic adaptation is fundamental for the function of the immune system and an individual's resistance to infection. We demonstrated that analogically to Drosophila, mammalian immune-activated macrophages produce ImpL2 homolog IGFBP7 in a HIF1α-dependent manner and that enhanced IGFBP7 production by these cells induces mobilization of lipoproteins from hepatocytes. Hence, the production of ImpL2/IGFBP7 by macrophages represents an evolutionarily conserved mechanism by which macrophages alleviate insulin signaling in the central metabolic organ to secure nutrients necessary for their function upon bacterial infection.
    Keywords:  Drosophila; ImpL2; insulin resistance; lipoproteins; macrophage polarization
    DOI:  https://doi.org/10.15252/embj.2023114086
  11. medRxiv. 2023 Sep 26. pii: 2023.09.25.23296086. [Epub ahead of print]
      Critical illness can disrupt the composition and function of the microbiome, yet comprehensive longitudinal studies are lacking. We conducted a longitudinal analysis of oral, lung, and gut microbiota in a large cohort of 479 mechanically ventilated patients with acute respiratory failure. Progressive dysbiosis emerged in all three body compartments, characterized by reduced alpha diversity, depletion of obligate anaerobe bacteria, and pathogen enrichment. Clinical variables, including chronic obstructive pulmonary disease, immunosuppression, and antibiotic exposure, shaped dysbiosis. Notably, of the three body compartments, unsupervised clusters of lung microbiota diversity and composition independently predicted survival, transcending clinical predictors, organ dysfunction severity, and host-response sub-phenotypes. These independent associations of lung microbiota may serve as valuable biomarkers for prognostication and treatment decisions in critically ill patients. Insights into the dynamics of the microbiome during critical illness highlight the potential for microbiota-targeted interventions in precision medicine.
    DOI:  https://doi.org/10.1101/2023.09.25.23296086
  12. Cytokine. 2023 Oct 11. pii: S1043-4666(23)00262-4. [Epub ahead of print]172 156384
      Fungal infections caused by Scedosporium species are rising among immunocompromised and immunocompetent patients. Within the immunocompetent group, patients with cystic fibrosis (pwCF) are at high risk of developing a chronic airway colonization by these molds. While S. apiospermum is one of the major species encountered in the lungs of pwCF, S. dehoogii has rarely been reported. The innate immune response is believed to be critical for host defense against fungal infections. However, its role has only recently been elucidated and the immune mechanisms against Scedosporium species are currently unknown. In this context, we undertook a comparative investigation of macrophage-mediated immune responses toward S. apiospermum and S. dehoogii conidia. Our data showed that S. apiospermum and S. dehoogii conidia strongly stimulated the expression of a set of pro-inflammatory cytokines and chemokines such as IL-1β, IL-8, IL-6 and TNFα. We demonstrated that S. dehoogii was more potent in stimulating the early release of pro-inflammatory cytokines and chemokines while S. apiospermum induced a late inflammatory response at a higher level. Flow cytometry analysis showed that M1-like macrophages were able to internalize both S. apiospermum and S. dehoogii conidia, with a similar intracellular killing rate for both species. In conclusion, these results suggest that M1-like macrophages can rapidly initiate a strong immune response against both S. apiospermum and S. dehoogii. This response is characterized by a similar killing of internalized conidia, but a different time course of cytokine production.
    Keywords:  Cytokines; Immune response; Inflammation; Macrophages; Scedosporium
    DOI:  https://doi.org/10.1016/j.cyto.2023.156384
  13. Microbes Infect. 2023 Oct 05. pii: S1286-4579(23)00140-5. [Epub ahead of print] 105237
      Methicillin-resistant Staphylococcus aureus (MRSA) isolated from patients with keratitis produces substantial amounts of phenol-soluble modulin α (PSMα). However, the role of PSMα in S. aureus keratitis remains unclear. We observed that PSMα-producing and PSMα-deficient strains could infect the cornea in our experimental mouse keratitis model; however, only the PSMα-producing strain induced delayed epithelial wound healing and stromal inflammation. PSMα induced damage to the epithelium, the release of alarmins IL-1α and IL-36α, and the expression of inflammatory chemokines by resident corneal cells in the mouse corneal organ culture. The IL-36 (but not IL-1) receptor antagonist attenuated mouse keratitis induced by PSMα-containing bacterial culture supernatants, as well as by infection with PSMα-producing S. aureus, suggesting that the corneal inflammations were dependent on IL-36. Recombinant PSMα elicited IL-36-dependent corneal inflammation in mice. Thus, PSMα and the subsequently released IL-36 are critical factors triggering inflammation during S. aureus keratitis.
    Keywords:  Staphylococcus aureus; alarmins; interleukin 36; keratitis; phenol-soluble modulin α; virulence
    DOI:  https://doi.org/10.1016/j.micinf.2023.105237
  14. Otolaryngol Clin North Am. 2023 Oct 10. pii: S0030-6665(23)00158-5. [Epub ahead of print]
      Allergy and asthma prevalence vary across different subsets of chronic rhinosinusitis with nasal polyposis. In this article, the authors investigate the management of allergy and asthma within populations of patients with aspirin-exacerbated respiratory disease, allergic fungal rhinosinusitis, and central compartment atopic disease. Topical steroids, nasal rinses, and endoscopic sinus surgery are frequently employed in the management of nasal polyposis. Further, other causes of upper and lower airway inflammation like allergy and asthma should be considered in the overall treatment plan in order to optimize outcomes.
    Keywords:  Allergic fungal rhinosinusitis; Allergy; Aspirin-exacerbated respiratory disease; Asthma; Central compartment atopic disease; Chronic sinusitis; Nasal polyps
    DOI:  https://doi.org/10.1016/j.otc.2023.09.001
  15. Int J Biol Macromol. 2023 Oct 04. pii: S0141-8130(23)04149-1. [Epub ahead of print] 127252
      Toll-like receptors play a vital role in cell-mediated immunity, which is crucial for the immune system's defense against pathogens and maintenance of homeostasis. The interaction between toll-like-receptor response and cell-mediated immunity is complex and essential for effectively eliminating pathogens and maintaining immune surveillance. In addition to pathogen recognition, toll-like receptors serve as adjuvants in vaccines, as molecular sensors, and recognize specific patterns associated with pathogens and danger signals. Incorporating toll-like receptor ligands into vaccines can enhance the immune response to antigens, making them potent adjuvants. Furthermore, they bridge the innate and adaptive immune systems and improve antigen-presenting cells' capacity to process and present antigens to T cells. The intricate signaling pathways and cross-talk between toll-like-receptor and T cell receptor (TCR) signaling emphasize their pivotal role in orchestrating effective immune responses against pathogens, thus facilitating the development of innovative vaccine strategies. This article provides an overview of the current understanding of toll-like receptor response and explores their potential clinical applications. By unraveling the intricate mechanisms of toll-like-receptor signaling, we can gain novel insights into immune responses and potentially develop innovative therapeutic approaches. Ongoing investigations into the toll-like-receptor response hold promise in the future in enhancing our ability to combat infections, design effective vaccines, and improve clinical outcomes.
    Keywords:  Cell-mediated immunity; T-cell; Toll-like receptors; vaccines
    DOI:  https://doi.org/10.1016/j.ijbiomac.2023.127252
  16. Front Immunol. 2023 ;14 1244431
      Although macrophages are known to be affected by their redox status, oxidation is not yet a well-recognized post-translational modification (PTM) in regulating macrophages and immune cells in general. While it has been described that the redox status of single cysteines in specific proteins is relevant for macrophage functions, global oxidation information is scarce. Hence, we globally assessed the impact of oxidation on macrophage activation using untargeted proteomics and PTM-omics. We exposed THP-1 macrophages to lipopolysaccharide (LPS) for 4 h and 24 h and applied a sequential iodoTMT labeling approach to get information on overall oxidation as well as reversible oxidation of cysteines. Thus, we identified 10452 oxidation sites, which were integratively analyzed with 5057 proteins and 7148 phosphorylation sites to investigate their co-occurance with other omics layers. Based on this integrative analysis, we found significant upregulation of several immune-related pathways, e.g. toll-like receptor 4 (TLR4) signaling, for which 19 proteins, 7 phosphorylation sites, and 39 oxidation sites were significantly affected, highlighting the relevance of oxidations in TLR4-induced macrophage activation. Co-regulation of oxidation and phosphorylation was observed, as evidenced by multiply modified proteins related to inflammatory pathways. Additionally, we observed time-dependent effects, with differences in the dynamics of oxidation sites compared to proteins and phosphorylation sites. Overall, this study highlights the importance of oxidation in regulating inflammatory processes and provides a method that can be readily applied to study the cellular redoxome globally.
    Keywords:  LPS; THP-1; phosphoproteome; proteome; redoxome
    DOI:  https://doi.org/10.3389/fimmu.2023.1244431
  17. Curr Opin Cell Biol. 2023 Oct 06. pii: S0955-0674(23)00105-9. [Epub ahead of print]85 102256
      In multicellular organisms, cell-to-cell communication is critical for the regulation of tissue organization. Notch signaling relies on direct interactions between Notch receptors on signal-receiving cells and Notch ligands on adjacent cells. Notch evolved to mediate local cellular interactions that are responsive to spatial cues via dosage-sensitive short-lived signals. Immune cells utilize these unique properties of Notch signaling to direct their development, differentiation, and function. In this review, we explore how immune cells interact through Notch receptors with stromal cells in specialized niches of lymphohematopoietic organs that express Notch-activating ligands. We emphasize factors that control these interactions and focus on how Notch signals communicate spatial, quantitative, and temporal information to program the function of signal-receiving cells in the immune system.
    DOI:  https://doi.org/10.1016/j.ceb.2023.102256
  18. Int J Mol Sci. 2023 Sep 25. pii: 14525. [Epub ahead of print]24(19):
      Macrophages are likely to be the first immune cells to have appeared during the evolution of multicellular organisms [...].
    DOI:  https://doi.org/10.3390/ijms241914525
  19. Int J Mol Sci. 2023 Sep 30. pii: 14789. [Epub ahead of print]24(19):
      The airway epithelium is a critical component of the respiratory system, serving as a barrier against inhaled pathogens and toxins. It is composed of various cell types, each with specific functions essential to proper airway function. Chronic respiratory diseases can disrupt the cellular composition of the airway epithelium, leading to a decrease in multiciliated cells (MCCs) and an increase in secretory cells (SCs). Basal cells (BCs) have been identified as the primary stem cells in the airway epithelium, capable of self-renewal and differentiation into MCCs and SCs. This review emphasizes the role of transcription factors in the differentiation process from BCs to MCCs and SCs. Recent advancements in single-cell RNA sequencing (scRNAseq) techniques have provided insights into the cellular composition of the airway epithelium, revealing specialized and rare cell types, including neuroendocrine cells, tuft cells, and ionocytes. Understanding the cellular composition and differentiation processes within the airway epithelium is crucial for developing targeted therapies for respiratory diseases. Additionally, the maintenance of BC populations and the involvement of Notch signaling in BC self-renewal and differentiation are discussed. Further research in these areas could provide valuable insights into the mechanisms underlying airway epithelial homeostasis and disease pathogenesis.
    Keywords:  Notch; airway epithelial cells; airway epithelium; multiciliated cells; secretory cells; transcription factors
    DOI:  https://doi.org/10.3390/ijms241914789
  20. Int J Mol Sci. 2023 Oct 03. pii: 14871. [Epub ahead of print]24(19):
      Cells are the smallest units that make up living organisms, which constantly undergo the processes of proliferation, differentiation, senescence and death. Dead cells need to be removed in time to maintain the homeostasis of the organism and keep it healthy. This process is called efferocytosis. If the process fails, this may cause different types of diseases. More and more evidence suggests that a faulty efferocytosis process is closely related to the pathological processes of respiratory diseases. In this review, we will first introduce the process and the related mechanisms of efferocytosis of the macrophage. Secondly, we will propose some methods that can regulate the function of efferocytosis at different stages of the process. Next, we will discuss the role of efferocytosis in different lung diseases and the related treatment approaches. Finally, we will summarize the drugs that have been applied in clinical practice that can act upon efferocytosis, in order to provide new ideas for the treatment of lung diseases.
    Keywords:  apoptosis; efferocytosis; macrophage; respiratory disease
    DOI:  https://doi.org/10.3390/ijms241914871
  21. Eur J Immunol. 2023 Oct 14. e2250348
      The importance of interleukin-23 (IL-23) and its specific receptor, IL-23R, in the pathogenesis of several chronic inflammatory diseases has been established, but the underlying pathological mechanisms are not fully understood. This review focuses on IL-23R expression and regulation. This article is protected by copyright. All rights reserved.
    Keywords:  Chronic inflammatory diseases; Gene regulation; Interleukin-23 (IL-23); Interleukin-23 receptor (IL-23R); Transcription factors
    DOI:  https://doi.org/10.1002/eji.202250348
  22. J Vis Exp. 2023 Sep 22.
      Three highly pathogenic human coronaviruses (HCoVs) - SARS-CoV (2002), MERS-CoV (2012), and SARS-CoV-2 (2019) - have emerged and caused significant public health crises in the past 20 years. Four additional HCoVs cause a significant portion of common cold cases each year (HCoV-NL63, -229E, -OC43, and -HKU1), highlighting the importance of studying these viruses in physiologically relevant systems. HCoVs enter the respiratory tract and establish infection in the nasal epithelium, the primary site encountered by all respiratory pathogens. We use a primary nasal epithelial culture system in which patient-derived nasal samples are grown at an air-liquid interface (ALI) to study host-pathogen interactions at this important sentinel site. These cultures recapitulate many features of the in vivo airway, including the cell types present, ciliary function, and mucus production. We describe methods to characterize viral replication, host cell tropism, virus-induced cytotoxicity, and innate immune induction in nasal ALI cultures following HCoV infection, using recent work comparing lethal and seasonal HCoVs as an example1. An increased understanding of host-pathogen interactions in the nose has the potential to provide novel targets for antiviral therapeutics against HCoVs and other respiratory viruses that will likely emerge in the future.
    DOI:  https://doi.org/10.3791/64868
  23. Cell Host Microbe. 2023 Oct 11. pii: S1931-3128(23)00374-8. [Epub ahead of print]31(10): 1569-1573
      Although environmental impacts on the host microbiome have been well studied, it is less certain whether and how host genetics impact the microbiome. This commentary discusses current literature supporting host genetic influences on resident species and pathogenic microbes. Mechanistic experimental studies are warranted to understand host gene-microbiome interplay.
    Keywords:  cancer; colon; colorectal cancer; gut; host genes; inflammatory bowel disease; inter-kingdom interactions; microbial evolution; microbiota; mutualism
    DOI:  https://doi.org/10.1016/j.chom.2023.09.007
  24. Trends Immunol. 2023 Oct 11. pii: S1471-4906(23)00206-5. [Epub ahead of print]
      Yolk sac-derived macrophages have been described to promote organogenesis and tissue function in animal models, but the relevance of these studies for humans has been debated. Wang et al. reveal that human macrophage development follows similar developmental trajectories with functionally distinct macrophage populations across tissues as observed in mice.
    DOI:  https://doi.org/10.1016/j.it.2023.09.010
  25. Microbiol Spectr. 2023 Oct 13. e0280723
      Genetic competence for natural transformation, considered one of the three main mechanisms leading to horizontal gene transfer in bacteria, is able to promote evolution, through genomic plasticity, and foster antibiotic resistance and virulence factors spreading. Conserved machinery and actors required to perform natural transformation have been shown to accumulate at different cellular localizations depending on the model organism considered. In this study, we investigate the transformation apparatus composition, localization, and dynamics in the human pathogen Staphylococcus aureus. We particularly show that most of the natural transformation actors co-localize in clusters. We also reveal that the localization of natural transformation proteins is dynamic, following the cell cycle. Ultimately, the natural transformation apparatus is preferentially established in the vicinity of the division septum. All these results demonstrate that DNA binding, uptake, and recombination are spatially and temporally coordinated to ensure S. aureus natural transformation. Finally, we hypothesize that S. aureus competent cells would initiate and then block cell division to ensure the success of natural transformation before the final constriction of the cytokinetic ring. IMPORTANCE Natural transformation, considered one of the three main mechanisms leading to horizontal gene transfer in bacteria, is able to promote genomic plasticity and foster antibiotic resistance spreading. Conserved machinery and actors required to perform natural transformation have been shown to accumulate at different cellular localizations depending on the model organism considered. Here, we show in the human pathogen Staphylococcus aureus that DNA binding, uptake, and recombination are spatially and temporally coordinated to ensure S. aureus natural transformation. We also reveal that localization of natural transformation proteins occurs in the vicinity of the division septum allowing S. aureus competent cells to block cell division to ensure the success of natural transformation before the final constriction of the cytokinetic ring.
    Keywords:  Staphylococcus aureus; cell cycle; division inhibition; genetic competence; horizonral gene transfer; natural transformation
    DOI:  https://doi.org/10.1128/spectrum.02807-23
  26. Gut Microbes. 2023 12;15(2): 2264456
      Several probiotic-derived factors have been identified as effectors of probiotics for exerting beneficial effects on the host. However, there is a paucity of studies to elucidate mechanisms of their functions. p40, a secretory protein, is originally isolated from a probiotic bacterium, Lactobacillus rhamnosus GG. Thus, this study aimed to apply structure-functional analysis to define the functional peptide of p40 that modulates the epigenetic program in intestinal epithelial cells for sustained prevention of colitis. In silico analysis revealed that p40 is composed of a signal peptide (1-28 residues) followed by a coiled-coil domain with uncharacterized function on the N-terminus, a linker region, and a β-sheet domain with high homology to CHAP on the C-terminus. Based on the p40 three-dimensional structure model, two recombinant p40 peptides were generated, p40N120 (28-120 residues) and p40N180 (28-180 residues) that contain first two and first three coiled coils, respectively. Compared to full-length p40 (p40F) and p40N180, p40N120 showed similar or higher effects on up-regulating expression of Setd1b (encoding a methyltransferase), promoting mono- and trimethylation of histone 3 on lysine 4 (H3K4me1/3), and enhancing Tgfb gene expression and protein production that leads to SMAD2 phosphorylation in human colonoids and a mouse colonic epithelial cell line. Furthermore, supplementation with p40F and p40N120 in early life increased H3K4me1, Tgfb expression and differentiation of regulatory T cells (Tregs) in the colon, and mitigated disruption of epithelial barrier and inflammation induced by DSS in adult mice. This study reveals the structural feature of p40 and identifies a functional peptide of p40 that could maintain intestinal homeostasis.
    Keywords:  Histone methyltransferase; Setd1β; TGFβ; intestinal epithelial cell; p40
    DOI:  https://doi.org/10.1080/19490976.2023.2264456
  27. J Inflamm (Lond). 2023 Oct 12. 20(1): 33
      When exposed to various microenvironmental stimuli, macrophages are highly plastic and primarily polarized into the pro-inflammatory M1-type and the anti-inflammatory M2-type, both of which perform almost entirely opposing functions. Due to this characteristic, macrophages perform different functions at different stages of immunity and inflammation. Inflammatory immune skin diseases usually show an imbalance in the M1/M2 macrophage ratio, and altering the macrophage polarization phenotype can either make the symptoms worse or better. Therefore, this review presents the mechanisms of macrophage polarization, inflammation-related signaling pathways (JAK/STAT, NF-κB, and PI3K/Akt), and the role of both in inflammatory immune skin diseases (psoriasis, AD, SLE, BD, etc.) to provide new directions for basic and clinical research of related diseases.
    Keywords:  Immunity; Inflammation; Macrophage polarization; Signaling pathway; Skin diseases
    DOI:  https://doi.org/10.1186/s12950-023-00360-z
  28. Cell Chem Biol. 2023 Oct 03. pii: S2451-9456(23)00326-4. [Epub ahead of print]
      Natural competence is the principal driver of streptococcal evolution. While acquisition of new traits could facilitate rapid fitness improvement for bacteria, entry into the competent state is a highly orchestrated event, involving an interplay between various pathways. We present a new type of competence-predation coordination mechanism in Streptococcus sanguinis. Unlike other streptococci that mediate competence through the ComABCDE regulon, several key components are missing in the S. sanguinis ComCDE circuitry. We assembled two synthetic biology devices linking competence-stimulating peptide (CSP) cleavage and export with a quantifiable readout to unravel the unique features of the S. sanguinis circuitry. Our results revealed the ComC precursor cleavage pattern and the two host ABC transporters implicated in the export of the S. sanguinis CSP. Moreover, we discovered a ComCDE-dependent bacteriocin locus. Overall, this study presents a mechanism for commensal streptococci to maximize transformation outcome in a fluid environment through extensive circuitry rewiring.
    Keywords:  Bacteriocin; Competence regulon; Competence stimulating peptide; Quorum sensing; Streptococcus sanguinis
    DOI:  https://doi.org/10.1016/j.chembiol.2023.09.007
  29. Cell Commun Signal. 2023 Oct 10. 21(1): 281
      BACKGROUND: Pyroptosis is crucial for controlling various immune cells. However, the role of allergen-induced CD11c + dendritic cell (DC) pyroptosis in allergic rhinitis (AR) remains unclear.METHODS: Mice were grouped into the control group, AR group and necrosulfonamide-treated AR group (AR + NSA group). The allergic symptom scores, OVA-sIgE titres, serum IL-1β/IL-18 levels, histopathological characteristics and T-helper cell-related cytokines were evaluated. CD11c/GSDMD-N-positive cells were examined by immunofluorescence analysis. Murine CD11c + bone marrow-derived DCs (BMDCs) were induced in vitro, stimulated with OVA/HDM, treated with necrosulfonamide (NSA), and further cocultured with lymphocytes to assess BMDC function. An adoptive transfer murine model was used to study the role of BMDC pyroptosis in allergic rhinitis.
    RESULTS: Inhibiting GSDMD-N-mediated pyroptosis markedly protected against Th1/Th2/Th17 imbalance and alleviated inflammatory responses in the AR model. GSDMD-N was mainly coexpressed with CD11c (a DC marker) in AR mice. In vitro, OVA/HDM stimulation increased pyroptotic morphological abnormalities and increased the expression of pyroptosis-related proteins in a dose-dependent manner; moreover, inhibiting pyroptosis significantly decreased pyroptotic morphology and NLRP3, C-Caspase1 and GSDMD-N expression. In addition, OVA-induced BMDC pyroptosis affected CD4 + T-cell differentiation and related cytokine levels, leading to Th1/Th2/Th17 cell imbalance. However, the Th1/Th2/Th17 cell immune imbalance was significantly reversed by NSA. Adoptive transfer of OVA-loaded BMDCs promoted allergic inflammation, while the administration of NSA to OVA-loaded BMDCs significantly reduced AR inflammation.
    CONCLUSION: Allergen-induced dendritic cell pyroptosis promotes the development of allergic rhinitis through GSDMD-N-mediated pyroptosis, which provides a clue to allergic disease interventions. Video Abstract.
    Keywords:  Allergic rhinitis; Dendritic cell; GSDMD-N; Pyroptosis
    DOI:  https://doi.org/10.1186/s12964-023-01309-8
  30. Front Cell Infect Microbiol. 2023 ;13 1286423
      
    Keywords:  bacterial pathogen; cellular recognition; host interaction; innate immunity; mechanisms of bacterial infection; protein-protein interaction; regulation; signaling
    DOI:  https://doi.org/10.3389/fcimb.2023.1286423
  31. Small. 2023 Oct 08. e2304940
      Organotypic 3D tissue models have greatly contributed to understand a wide range of molecular and cellular characteristics within a functional or diseased tissue. Human skin reconstructs which act as models are most useful for a wide range of investigations, ranging from tissue engineering and regenerative medicine, drug development, screening, and discovery to name a few. There are many approaches for reconstructing 3D skin tissue models, however, to date there have been very few that are able to generate organotypic 3D constructs with a single technology having minimal processing steps to finally scalability. The many manifestations of 3D bioprinting have contributed to this endeavor, having said that, the technology's limitations have tempered those reconstructed models, as they are known to contain low cell numbers/concentrations to those having damaged/dead molecules/cells within the reconstructed tissue, which are not desirable, for exploring as tissues models. Contrary to 3D bioprinting approaches, bio-electrosprays have been demonstrated to possess the ability to handle large concentrations of cells and molecules to whole fertilized embryos without damaging them from a molecular level upwards. Consequently, this article demonstrates, for the first time, bio-electrospray's capacity to reconstruct skin-like structures in vitro and its potential in reconstructing full-thickness 3D organotypic human skin tissues.
    Keywords:  additive biomanufacturing; bio-electrosprays; biological models; cells ; organotypic 3D human skin tissue; skin cultures
    DOI:  https://doi.org/10.1002/smll.202304940
  32. Int J Mol Sci. 2023 Oct 05. pii: 14935. [Epub ahead of print]24(19):
      Respiratory diseases have a major impact on global health. The airway epithelium, which acts as a frontline defence, is one of the most common targets for inhaled allergens, irritants, or micro-organisms to enter the respiratory system. In the tissue engineering field, biomaterials play a crucial role. Due to the continuing high impact of respiratory diseases on society and the emergence of new respiratory viruses, in vitro airway epithelial models with high microphysiological similarities that are also easily adjustable to replicate disease models are urgently needed to better understand those diseases. Thus, the development of biomaterial scaffolds for the airway epithelium is important due to their function as a cell-support device in which cells are seeded in vitro and then are encouraged to lay down a matrix to form the foundations of a tissue for transplantation. Studies conducted in in vitro models are necessary because they accelerate the development of new treatments. Moreover, in comparatively controlled conditions, in vitro models allow for the stimulation of complex interactions between cells, scaffolds, and growth factors. Based on recent studies, the biomaterial scaffolds that have been tested in in vitro models appear to be viable options for repairing the airway epithelium and avoiding any complications. This review discusses the role of biomaterial scaffolds in in vitro airway epithelium models. The effects of scaffold, physicochemical, and mechanical properties in recent studies were also discussed.
    Keywords:  airway epithelium; biomaterial; in vitro; mucociliary differentiation; scaffold
    DOI:  https://doi.org/10.3390/ijms241914935
  33. Nature. 2023 Oct 13.
      
    Keywords:  Microbiome
    DOI:  https://doi.org/10.1038/d41586-023-03105-3
  34. Georgian Med News. 2023 Jul-Aug;(340-341): 153-158
      The diverse population of microbes that live in our digestive system, known as the gut microbiota, remains essential for many physiological processes. It plays a role in obtaining energy from food and controls both regional and overall immunity. In addition, changes in the microbiota of the digestive tract are connected to the emergence of an extensive variety of illnesses, such as cancer, gastrointestinal problems, and metabolic disorders. From a metabolic perspective, the gut microbiota can affect processes like lipid accumulation, lipopolysaccharide satisfied, and short-chain fatty acid synthesis, all of which have an effect on food intake, inflammatory reactions, and insulin signaling. Prebiotics, probiotics, specialized anti-diabetic medications, and faecalmicrobiota implantation are a few of the ways that have been discovered to alter the gut microbiota; each has a different influence the human body's metabolism and the emergence of metabolic disorders. These therapies have been reported to be therapeutic strategies for enhancing general wellness and reestablishing a balanced gut flora.
  35. J Virol. 2023 Oct 11. e0127123
      Respiratory mucus lining the airway epithelium constitutes an important first line of defense against infection with influenza A virus (IAV). Previous studies suggested that the inhibitory potential of mucus relies not only on the presence of decoy receptors but also on the dense meshwork blocking virus access to the epithelium independent of sialic acid. Here, we report for a panel of human and avian IAV isolates that susceptibility to neutralization by respiratory mucus varies in a strain-dependent manner. Our data reveal that viral neuraminidase (NA) activity inversely correlates with the mucus sensitivity of a given strain. As NA cleaves sialic acid from glycan chains and thus releases IAV from decoy receptor binding, our results imply that virus inhibition by mucus is mainly driven by decoy receptor binding of IAV. Other inhibitory properties of mucus, such as size exclusion, non-covalent interactions with mucus components, or the presence of immunomodulatory molecules, likely play minor roles in neutralizing IAV. Inhibition of NA activity using oseltamivir was sufficient to increase the sensitivity of a seasonal IAV strain to mucus during infection in a cell-based neutralization assay and in differentiated primary human airway epithelial cultures. Overall, our data highlight the importance of NA for the initiation of virus infection besides its major function in release, especially in overcoming the host defense mechanism of mucociliary clearance in the airway epithelium. Furthermore, strain-specific differences in the ability to penetrate respiratory mucus may be the result of host adaptation and can have consequences for the transmissibility and infectivity of circulating viruses. IMPORTANCE The respiratory tract of humans is constantly exposed to potentially harmful agents, such as small particles or pathogens, and thus requires protective measures. Respiratory mucus that lines the airway epithelia plays a major role in the prevention of viral infections by limiting the mobility of viruses, allowing subsequent mucociliary clearance. Understanding the interplay between respiratory mucus and viruses can help elucidate host and virus characteristics that enable the initiation of infection. Here, we tested a panel of primary influenza A viruses of avian or human origin for their sensitivity to mucus derived from primary human airway cultures and found that differences between virus strains can be mapped to viral neuraminidase activity. We also show that binding of influenza A viruses to decoy receptors on highly glycosylated mucus components constitutes the major inhibitory function of mucus against influenza A viruses.
    Keywords:  influenza; mucus; neutralization
    DOI:  https://doi.org/10.1128/jvi.01271-23
  36. Integr Zool. 2023 Oct 10.
      The importance of issues associated with urban/commensal rats and mice (property damage, management costs, and health risks) press upon research on these animals. While the demography of commensal rodents is mostly studied, the need for understanding factors influencing their natural morbidity/mortality is also stressed. In this respect, more attention is expected to be paid to immunity, the physiological mechanism of defense against host survival threats (pathogens, parasites, diseases). Commensal rats and mice carry numerous pathogens that evoke diverse immune responses. The state of immunity in commensal house mice is studied in great detail, owing to the use of laboratory strains in biomedical research. Because commensal rats are, compared to mice, carriers of more zoonotic agents, rats' immunity is studied mainly in that context. Some of these zoonotic agents cause chronic, asymptomatic infections, which justified studies of immunological mechanisms of pathogen tolerance versus clearance regulation in rats. Occurrence of some infections in specific tissues/organs pressed upon analysis of local/regional immune responses and/or immunopathology. A survey of immunological activity/responses in commensal rats is given in this review, with mention of existing data in commensal mice. It should throw some light on the factors relevant to their morbidity and lifespan, supplementing the knowledge of commensal rodent ecology.
    Keywords:  commensal rats and mice; immunopathology; infection; inflammation; tolerance
    DOI:  https://doi.org/10.1111/1749-4877.12766
  37. Front Genet. 2023 ;14 1290552
      
    Keywords:  circadian; circannual; immunity; microbiome; physiology
    DOI:  https://doi.org/10.3389/fgene.2023.1290552
  38. Gut Microbes. 2023 Dec;15(2): 2267706
      Microbiota-derived short-chain fatty acids, including butyrate (BA), have multiple beneficial health effects. In the colon, BA concentrations range from 10 to 20 mM and up to 95% is utilized as energy by the mucosa. BA plays a key role in epithelial-barrier regulation and anti-inflammation, and regulates cell growth and differentiation, at least in part, due to its direct influence on stabilization of the transcription factor hypoxia-inducible factor (HIF). It remains unclear whether BA is the optimal metabolite for such a response. In this study, we explored metabolite mimicry as an attractive strategy for the biological response to HIF. We discovered that 4-mercapto butyrate (MBA) stabilizes HIF more potently and has a longer biological half-life than BA in intestinal epithelial cells (IECs). We validated the MBA-mediated HIF transcriptional activity through the induction of classic HIF gene targets in IECs and enhanced epithelial barrier formation in vitro. In-vivo studies with MBA revealed systemic HIF stabilization in mice, which was more potent than its parent BA metabolite. Mechanistically, we found that MBA enhances oxygen consumption and that the sulfhydryl group is essential for HIF stabilization, but exclusively as a four-carbon SCFA. These findings reveal a combined biochemical mechanism for HIF stabilization and provide a foundation for the discovery of potent metabolite-like scaffolds.
    Keywords:  HIF; Metabolism; butyrate; hypoxia; inflammation; microbiota; mucosa
    DOI:  https://doi.org/10.1080/19490976.2023.2267706
  39. iScience. 2023 Oct 20. 26(10): 107889
      This study characterized mechanisms of Bacille Calmette-Guérin (BCG) revaccination-induced trained immunity (TI) in India. Adults, BCG vaccinated at birth, were sampled longitudinally before and after a second BCG dose. BCG revaccination significantly elevated tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, and IL-6 in HLA-DR+CD16-CD14hi monocytes, demonstrating induction of TI. Mycobacteria-specific CD4+ T cell interferon (IFN) γ, IL-2, and TNF-α were significantly higher in re-vaccinees and correlated positively with HLA-DR+CD16-CD14hi TI responses. This, however, did not translate into increased mycobacterial growth control, measured by mycobacterial growth inhibition assay (MGIA). Post revaccination, elevated secreted TNF-α, IL-1β, and IL-6 to "heterologous" fungal, bacterial, and enhanced CXCL-10 and IFNα to viral stimuli were also observed concomitant with increased anti-inflammatory cytokine, IL-1RA. RNA sequencing after revaccination highlighted a BCG and LPS induced signature which included upregulated IL17 and TNF pathway genes and downregulated key inflammatory genes: CXCL11, CCL24, HLADRA, CTSS, CTSC. Our data highlight a balanced immune response comprising pro- and anti-inflammatory mediators to be a feature of BCG revaccination-induced immunity.
    Keywords:  Immune response; Immunity; Immunology; Molecular biology; Omics; Transcriptomics
    DOI:  https://doi.org/10.1016/j.isci.2023.107889