bims-bac4me Biomed News
on Microbiome and trained immunity
Issue of 2023‒06‒25
twenty-two papers selected by
Chun-Chi Chang
University Hospital Zurich


  1. Mol Pharm. 2023 Jun 21.
      Microorganisms that make up the local microbiota (such as Lactobacillus sp. and Bifidobacterium sp.) play a crucial role in the modulation of diseases and health states by taking place not only in the gut but also in many parts of our body. There is also interference between the gut and the lung via the gut-lung axis. The relationship between respiratory diseases and lung microbiota, which become more of an issue of particular importance in recent years, shows that probiotics play an essential role in maintaining the balance of microorganisms in the respiratory tract. However, studies on probiotics' prophylactic or therapeutic application in chronic lung diseases are limited. In this review, the literature between 1977 and 2022 was surveyed. General information about human microbiota was accessed in earlier sources, and especially in the past decade, research on lung microbiota has been reached. The relationship between lung microbiota and important respiratory diseases such as bronchopulmonary dysplasia, chronic obstructive pulmonary disease, pneumonia, cystic fibrosis, allergy-asthma, influenza, lung cancer, and COVID-19 infection, was scrutinized after mentioning human microbiota, the gut-lung axis, and respiratory tract microbiota. The mechanism of action of probiotics and the formulation approaches of probiotics in terms of pharmaceutical technology were reviewed. Finally, future perspectives on lung-targeted administration of probiotic bacteria with prophylactic or therapeutic potential, or both, were presented.
    Keywords:  Lactobacillus; chronic lung diseases; lung microbiota; microencapsulation; probiotic technology; probiotics; respiratory tract
    DOI:  https://doi.org/10.1021/acs.molpharmaceut.3c00323
  2. Microbiol Spectr. 2023 Jun 21. e0259021
      Staphylococcus aureus carriage is a risk factor for invasive infections. Unique genetic elements favoring the transition from colonizing to invasive phenotype have not yet been identified, and phenotypic adaptation traits are understudied. We therefore assessed phenotypic and genotypic profiles of 11 S. aureus isolate pairs sampled from colonized patients simultaneously suffering from invasive S. aureus infections. Ten out of 11 isolate pairs displayed the same spa and multilocus sequence type, suggesting colonization as an origin for the invasive infection. Systematic analysis of colonizing and invasive isolate pairs showed similar adherence, hemolysis, reproductive fitness properties, antibiotic tolerance, and virulence in a Galleria mellonella infection model, as well as minimal genetic differences. Our results provide insights into the similar phenotypes associated with limited adaptation between colonizing and invasive isolates. Disruption of the physical barriers of mucosa or skin was identified in the majority of patients, further emphasizing colonization as a major risk factor for invasive disease. IMPORTANCE S. aureus is a major pathogen of humans, causing a wide range of diseases. The difficulty to develop a vaccine and antibiotic treatment failure warrant the exploration of novel treatment strategies. Asymptomatic colonization of the human nasal passages is a major risk factor for invasive disease, and decolonization procedures have been effective in preventing invasive infections. However, the transition of S. aureus from a benign colonizer of the nasal passages to a major pathogen is not well understood, and both host and bacterial properties have been discussed as being relevant for this behavioral change. We conducted a thorough investigation of patient-derived strain pairs reflecting colonizing and invasive isolates in a given patient. Although we identified limited genetic adaptation in certain strains, as well as slight differences in adherence capacity among colonizing and invasive isolates, our work suggests that barrier breaches are a key event in the disease continuum of S. aureus.
    Keywords:  Staphylococcus aureus; barrier breach; colonization; fitness; genomics; invasive infection; transition; upper respiratory tract
    DOI:  https://doi.org/10.1128/spectrum.02590-21
  3. Cell Rep. 2023 Jun 16. pii: S2211-1247(23)00669-1. [Epub ahead of print]42(6): 112658
      Itaconate is an immunomodulatory metabolite produced by immune cells under microbial stimulation and certain pro-inflammatory conditions and triggers antioxidant and anti-inflammatory responses. We show that dimethyl itaconate, a derivative of itaconate previously linked to suppression of inflammation and widely employed as an alternative to the endogenous metabolite, can induce long-term transcriptional, epigenomic, and metabolic changes, characteristic of trained immunity. Dimethyl itaconate alters glycolytic and mitochondrial energetic metabolism, ultimately leading to increased responsiveness to microbial ligand stimulation. Subsequently, mice treated with dimethyl itaconate present increased survival to infection with Staphylococcus aureus. Additionally, itaconate levels in human plasma correlate with enhanced ex vivo pro-inflammatory cytokine production. Collectively, these findings demonstrate that dimethyl itaconate displays short-term anti-inflammatory characteristics and the capacity to induce long-term trained immunity. This pro-and anti-inflammatory dichotomy of dimethyl itaconate is likely to induce complex immune responses and should be contemplated when considering itaconate derivatives in a therapeutic context.
    Keywords:  CP: Immunology; glutathione; infection; innate immunity; itaconate; metabolism; monocytes; trained immunity
    DOI:  https://doi.org/10.1016/j.celrep.2023.112658
  4. J Adv Res. 2023 Jun 21. pii: S2090-1232(23)00171-6. [Epub ahead of print]
      INTRODUCTION: Epidemiological evidences reveal that populations with psychological stress have an increased likelihood of respiratory viral infection involving influenza A virus (IAV) and SARS-CoV-2.OBJECTIVES: This study aims to explore the potential correlation between psychological stress and increased susceptibility to respiratory viral infections and how this may contribute to a more severe disease progression.
    METHODS: A chronic restraint stress (CRS) mouse model was used to infect IAV and estimate lung inflammation. Alveolar macrophages (AMs) were observed in the numbers, function and metabolic-epigenetic properties. To confirm the central importance of the gut microbiome in stress-exacerbated viral pneumonia, mice were conducted through microbiome depletion and gut microbiome transplantation.
    RESULTS: Stress exposure induced a decline in Lactobacillaceae abundance and hence γ-aminobutyric acid (GABA) level in mice. Microbial-derived GABA was released in the peripheral and sensed by AMs via GABAAR, leading to enhanced mitochondrial metabolism and α-ketoglutarate (αKG) generation. The metabolic intermediator in turn served as the cofactor for the epigenetic regulator Tet2 to catalyze DNA hydroxymethylation and promoted the PPARγ-centered gene program underpinning survival, self-renewing, and immunoregulation of AMs. Thus, we uncover an unappreciated GABA/Tet2/PPARγ regulatory circuitry initiated by the gut microbiome to instruct distant immune cells through a metabolic-epigenetic program. Accordingly, reconstitution with GABA-producing probiotics, adoptive transferring of GABA-conditioned AMs, or resumption of pulmonary αKG level remarkably improved AMs homeostasis and alleviated severe pneumonia in stressed mice.
    CONCLUSION: Together, our study identifies microbiome-derived tonic signaling tuned by psychological stress to imprint resident immune cells and defensive response in the lungs. Further studies are warranted to translate these findings, basically from murine models, into the individuals with psychiatric stress during respiratory viral infection.
    Keywords:  GABA; alveolar macrophages; gut microbiome; psychological stress; respiratory viral infection
    DOI:  https://doi.org/10.1016/j.jare.2023.06.008
  5. mBio. 2023 Jun 20. e0085423
      Acute respiratory infections are the most frequent infections across the lifespan and are the leading infectious cause of death among children globally. Bacterial respiratory infections are routinely treated with antibiotics, nearly all of which are derived from microbial natural products. Unfortunately, antibiotic-resistant bacteria are an increasingly frequent cause of respiratory infections, and there are few new antibiotics in development that target these pathogens. In the article by Stubbendieck et al., the authors identified Rothia species that demonstrate in vitro and ex vivo growth inhibition of the respiratory pathobiont Moraxella catarrhalis. The authors present experiments suggesting that this activity is mediated at least in part through the secretion of a novel peptidoglycan endopeptidase that targets the M. catarrhalis cell wall. In this commentary, we discuss these findings in the context of the urgent threat of antimicrobial resistance and highlight the promise of the human respiratory microbiota as a source of novel biotherapeutics.
    Keywords:  Moraxella catarrhalis; Rothia species; acute otitis media; antibiotic resistance; comparative genomics; human microbiome; microbial ecology; respiratory pathogens
    DOI:  https://doi.org/10.1128/mbio.00854-23
  6. FEMS Microbes. 2022 ;3 xtac020
      Emerging evidence suggests that the nasal microbiome may influence host susceptibility to initial development and severity of respiratory viral infections. While not as extensively studied as the microbiota of the alimentary tract, it is now clearly established that the microbial composition of this niche is influenced by medical, social and pharmacological influences, predisposing some sub-populations to respiratory infections. The resulting specific microbial profiles may explain variance in susceptibility to viral infection. This review summaries the evolution and constituents of the commensal nasal microbiome; the bacterial-virus, bacterial-host and interbacterial interactions which potentiate disease; and considers the effects of interventions such as vaccination and probiotics.
    Keywords:  bacteria; commensal; nasal cavity; nasopharynx; respiratory; viruses
    DOI:  https://doi.org/10.1093/femsmc/xtac020
  7. J Extracell Vesicles. 2023 06;12(6): e12335
      Filaggrin (FLG) protein is indispensable for multiple aspects of the epidermal barrier function but its accumulation in a monomeric filaggrin form may initiate premature keratinocytes death; it is unclear how filaggrin levels are controlled before the formation of storing keratohyalin granules. Here we show that keratinocyte-secreted small extracellular vesicles (sEVs) may contain filaggrin-related cargo providing a route of eliminating excess filaggrin from keratinocytes; blocking of sEV release has cytotoxic effects on those cells. Filaggrin-containing sEVs are found in plasma in both healthy individuals and atopic dermatitis patients. Staphylococcus aureus (S. aureus) enhances packaging and secretion of filaggrin-relevant products within the sEVs for enhanced export via a TLR2-mediated mechanism which is also linked to the ubiquitination process. This filaggrin removal system, preventing premature keratinocyte death and epidermal barrier dysfunction, is exploited by S. aureus which promotes filaggrin elimination from the skin that could help safeguard bacterial growth.
    Keywords:  Staphylococcus aureus; atopic dermatitis; bacteria; exosomes; extracellular vesicles; filaggrin; keratinocyte
    DOI:  https://doi.org/10.1002/jev2.12335
  8. Nature. 2023 Jun;618(7966): 698-707
      Embryo-derived tissue-resident macrophages are the first representatives of the haematopoietic lineage to emerge in metazoans. In mammals, resident macrophages originate from early yolk sac progenitors and are specified into tissue-specific subsets during organogenesis-establishing stable spatial and functional relationships with specialized tissue cells-and persist in adults. Resident macrophages are an integral part of tissues together with specialized cells: for instance, microglia reside with neurons in brain, osteoclasts reside with osteoblasts in bone, and fat-associated macrophages reside with white adipocytes in adipose tissue. This ancillary cell type, which is developmentally and functionally distinct from haematopoietic stem cell and monocyte-derived macrophages, senses and integrates local and systemic information to provide specialized tissue cells with the growth factors, nutrient recycling and waste removal that are critical for tissue growth, homeostasis and repair. Resident macrophages contribute to organogenesis, promote tissue regeneration following damage and contribute to tissue metabolism and defence against infectious disease. A correlate is that genetic or environment-driven resident macrophage dysfunction is a cause of degenerative, metabolic and possibly inflammatory and tumoural diseases. In this Review, we aim to provide a conceptual outline of our current understanding of macrophage physiology and its importance in human diseases, which may inform and serve the design of future studies.
    DOI:  https://doi.org/10.1038/s41586-023-06002-x
  9. bioRxiv. 2023 Jun 09. pii: 2023.06.09.543079. [Epub ahead of print]
      To cause infection, pathogens must overcome bottlenecks imposed by the host immune system. These bottlenecks restrict the inoculum and largely determine whether pathogen exposure results in disease. Infection bottlenecks therefore quantify the effectiveness of immune barriers. Here, using a model of Escherichia coli systemic infection, we identify bottlenecks that tighten or widen with higher inoculum sizes, revealing that the efficacy of innate immune responses can increase or decrease with pathogen dose. We term this concept "dose scaling". During E. coli systemic infection, dose scaling is tissue specific, dependent on the LPS receptor TLR4, and can be recapitulated by mimicking high doses with killed bacteria. Scaling is therefore due to sensing of pathogen molecules rather than interactions between the host and live bacteria. We propose that dose scaling quantitatively links innate immunity with infection bottlenecks and is a valuable framework for understanding how the inoculum size governs the outcome of pathogen exposure.
    DOI:  https://doi.org/10.1101/2023.06.09.543079
  10. Sci Rep. 2023 Jun 22. 13(1): 10137
      The human airways are complex structures with important interactions between cells, extracellular matrix (ECM) proteins and the biomechanical microenvironment. A robust, well-differentiated in vitro culture system that accurately models these interactions would provide a useful tool for studying normal and pathological airway biology. Here, we report the development and characterization of a physiologically relevant air-liquid interface (ALI) 3D airway 'organ tissue equivalent' (OTE) model with three novel features: native pulmonary fibroblasts, solubilized lung ECM, and hydrogel substrate with tunable stiffness and porosity. We demonstrate the versatility of the OTE model by evaluating the impact of these features on human bronchial epithelial (HBE) cell phenotype. Variations of this model were analyzed during 28 days of ALI culture by evaluating epithelial confluence, trans-epithelial electrical resistance, and epithelial phenotype via multispectral immuno-histochemistry and next-generation sequencing. Cultures that included both solubilized lung ECM and native pulmonary fibroblasts within the hydrogel substrate formed well-differentiated ALI cultures that maintained a barrier function and expressed mature epithelial markers relating to goblet, club, and ciliated cells. Modulation of hydrogel stiffness did not negatively impact HBE differentiation and could be a valuable variable to alter epithelial phenotype. This study highlights the feasibility and versatility of a 3D airway OTE model to model the multiple components of the human airway 3D microenvironment.
    DOI:  https://doi.org/10.1038/s41598-023-36863-1
  11. Exp Dermatol. 2023 Jun 23.
      Two major arms of skin ageing are changes in the skin's biophysical conditions and alterations in the skin microbiome. This work partitioned both arms to study their interaction in detail. Leveraging the resolution provided by shotgun metagenomics, we explored how skin microbial species, strains and gene content interact with the biophysical traits of the skin during ageing. With a dataset well-controlled for confounding factors, we found that skin biophysical traits, especially the collagen diffusion coefficient, are associated with the composition and the functional potential of the skin microbiome, including the abundance of bacterial strains found in nosocomial infections and the abundance of antibiotic resistance genes. Our findings reveal important associations between skin biophysical features and ageing-related changes in the skin microbiome and generate testable hypotheses for the mechanisms of such associations.
    Keywords:  collagen; microbiota; skin; skin ageing
    DOI:  https://doi.org/10.1111/exd.14863
  12. Cell Rep. 2023 Jun 19. pii: S2211-1247(23)00659-9. [Epub ahead of print]42(6): 112648
      Polysialic acid (polySia) is a post-translational modification of a select group of cell-surface proteins that guides cellular interactions. As the overall impact of changes in expression of this glycan on leukocytes during infection is not known, we evaluate the immune response of polySia-deficient ST8SiaIV-/- mice infected with Streptococcus pneumoniae (Spn). Compared with wild-type (WT) mice, ST8SiaIV-/- mice are less susceptible to infection and clear Spn from airways faster, with alveolar macrophages demonstrating greater viability and phagocytic activity. Leukocyte pulmonary recruitment, paradoxically, is diminished in infected ST8SiaIV-/- mice, corroborated by adoptive cell transfer, microfluidic migration experiments, and intravital microscopy, and possibly explained by dysregulated ERK1/2 signaling. PolySia is progressively lost from neutrophils and monocytes migrating from bone marrow to alveoli in Spn-infected WT mice, consistent with changing cellular functions. These data highlight multidimensional effects of polySia on leukocytes during an immune response and suggest therapeutic interventions for optimizing immunity.
    Keywords:  CP: Immunology; Streptococcus pneumoniae; extracellular signal-regulated kinase ERK1/2; intravital microscopy; leukocyte migration; microfluidic migration chambers; monocytes; neutrophils; phagocytosis; polysialic acid; polysialyltransferase ST8SiaIV
    DOI:  https://doi.org/10.1016/j.celrep.2023.112648
  13. bioRxiv. 2023 Jun 07. pii: 2023.06.06.543868. [Epub ahead of print]
      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 -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 sputum (CF) 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 (padj < 0.05, fold-change >2). Higher expression of antibiotic resistance and biofilm functions were 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 ( P = -0.43) and CF ( P = -0.27) samples and they significantly contributed to the expression of these functions. Additionally, we show microbial communities have unique expression patterns and distinct organisms fulfill the expression of key functions in each site, indicating 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 is lacking. Here, we highlight that the predominant functions in chronic PMIs differ, and anaerobes, often described as contaminants, may be significant in the progression of chronic infections. Determining the community structure and functions in PMIs is a critical step towards understanding the molecular mechanisms that drive microbe-microbe interactions in these environments.
    DOI:  https://doi.org/10.1101/2023.06.06.543868
  14. Angew Chem Int Ed Engl. 2023 Jun 22. e202306427
      Staphylococcus aureus (S. aureus) is able to hide within host cells to escape immune clearance and antibiotic action, causing life-threatening infections. To boost the therapeutic efficacy of antibiotics, new intracellular delivery approaches are urgently needed. Herein, by rational design of an adamantane (Ada)-containing antibiotic-peptide precursor Ada-Gly-Tyr-Val-Ala-Asp-Cys(StBu)-Lys(Ciprofloxacin)-CBT (Cip-CBT-Ada), we propose a strategy of tandem guest-host-receptor recognitions to precisely guide ciprofloxacin to eliminate intracellular S. aureus. Via guest-host recognition, Cip-CBT-Ada is decorated with a β-cyclodextrin-heptamannoside (CD-M) derivative to yield Cip-CBT-Ada/CD-M, which is able to target mannose receptor-overexpressing macrophages via multivalent ligand-receptor recognition. After uptake, Cip-CBT-Ada/CD-M undergoes caspase-1 (an overexpressed enzyme during S. aureus infection)-initiated CBT-Cys click reaction to self-assemble into ciprofloxacin nanoparticle Nano-Cip. In vitro and in vivo experiments demonstrate that, compared with ciprofloxacin or Cip-CBT-Ada, Cip-CBT-Ada/CD-M shows superior intracellular bacteria elimination and inflammation alleviation efficiency in S. aureus-infected RAW264.7 cells and mouse infection models, respectively. This work provides a supramolecular platform of tandem guest-host-receptor recognitions to precisely guide antibiotics to eliminate intracellular S. aureus infection efficiently.
    Keywords:  Host-guest interaction; antimicrobials; caspase-1; nanoparticle; self-assembly
    DOI:  https://doi.org/10.1002/anie.202306427
  15. Sci Immunol. 2023 Jun 23. 8(84): eadd6910
      The paucity of blood granulocyte populations such as neutrophils in laboratory mice is a notable difference between this model organism and humans, but the cause of this species-specific difference is unclear. We previously demonstrated that laboratory mice released into a seminatural environment, referred to as rewilding, display an increase in blood granulocytes that is associated with expansion of fungi in the gut microbiota. Here, we find that tonic signals from fungal colonization induce sustained granulopoiesis through a mechanism distinct from emergency granulopoiesis, leading to a prolonged expansion of circulating neutrophils that promotes immunity. Fungal colonization after either rewilding or oral inoculation of laboratory mice with Candida albicans induced persistent expansion of myeloid progenitors in the bone marrow. This increase in granulopoiesis conferred greater long-term protection from bloodstream infection by gram-positive bacteria than by the trained immune response evoked by transient exposure to the fungal cell wall component β-glucan. Consequently, introducing fungi into laboratory mice may restore aspects of leukocyte development and provide a better model for humans and free-living mammals that are constantly exposed to environmental fungi.
    DOI:  https://doi.org/10.1126/sciimmunol.add6910
  16. Sci Adv. 2023 Jun 23. 9(25): eadg8719
      Animals evolved two defense strategies to survive infections. Antagonistic strategies include immune resistance mechanisms that operate to kill invading pathogens. Cooperative or physiological defenses mediate host adaptation to the infected state, limiting physiological damage and disease, without killing the pathogen, and have been shown to cause asymptomatic carriage and transmission of lethal pathogens. Here, we demonstrate that physiological defenses cooperate with the adaptive immune response to generate long-term asymptomatic carriage of the lethal enteric murine pathogen, Citrobacter rodentium. Asymptomatic carriage of genetically virulent C. rodentium provided immune resistance against subsequent infections. Immune protection was dependent on systemic antibody responses and pathogen virulence behavior rather than the recognition of specific virulent antigens. Last, we demonstrate that an avirulent strain of C. rodentium in the field has background mutations in genes that are important for LPS structure. Our work reveals insight into how asymptomatic infections can arise mechanistically with immune resistance, mediating exclusion of phenotypically virulent enteric pathogen to promote asymptomatic carriage.
    DOI:  https://doi.org/10.1126/sciadv.adg8719
  17. J Allergy Clin Immunol. 2023 Jun 19. pii: S0091-6749(23)00800-X. [Epub ahead of print]
      The ability of human tissue to reorganize and restore its existing structure underlies tissue homeostasis in the healthy airways, but in disease can persist without normal resolution, leading to an altered airway structure. Eosinophils play a cardinal role in airway remodeling both in health and disease, driving epithelial homeostasis and extracellular matrix turnover. Physiological consequences associated with eosinophil-driven remodeling include impaired lung function and reduced bronchodilator reversibility in asthma, and obstructed airflow in chronic rhinosinusitis with nasal polyps (CRSwNP). Given the contribution of airway remodeling to the development and persistence of symptoms in airways disease, targeting remodeling is an important therapeutic consideration. Indeed, there is early evidence that eosinophil attenuation may reduce remodeling and disease progression in asthma. This review provides an overview of tissue remodeling in both health and airway disease with a particular focus on eosinophilic asthma and CRSwNP, as well as the role of eosinophils in these processes and the implications for therapeutic interventions. Areas for future research are also noted, to help improve our understanding of the homeostatic and pathological roles of eosinophils in tissue remodeling, which should aid the development of targeted and effective treatments for eosinophilic diseases of the airways.
    Keywords:  Airway remodeling; asthma; chronic rhinosinusitis with nasal polyps; eosinophil
    DOI:  https://doi.org/10.1016/j.jaci.2023.06.005
  18. Intensive Care Med Exp. 2023 Jun 23. 11(1): 34
    SCORPIUS study group
      
    Keywords:  Anaerobes; Respiratory microbiota; Staphylococcus aureus; Ventilator-associated pneumonia
    DOI:  https://doi.org/10.1186/s40635-023-00521-7
  19. Nat Commun. 2023 Jun 17. 14(1): 3614
      Many medications can negatively impact the bacteria residing in our gut, depleting beneficial species, and causing adverse effects. To guide personalized pharmaceutical treatment, a comprehensive understanding of the impact of various drugs on the gut microbiome is needed, yet, to date, experimentally challenging to obtain. Towards this end, we develop a data-driven approach, integrating information about the chemical properties of each drug and the genomic content of each microbe, to systematically predict drug-microbiome interactions. We show that this framework successfully predicts outcomes of in-vitro pairwise drug-microbe experiments, as well as drug-induced microbiome dysbiosis in both animal models and clinical trials. Applying this methodology, we systematically map a large array of interactions between pharmaceuticals and human gut bacteria and demonstrate that medications' anti-microbial properties are tightly linked to their adverse effects. This computational framework has the potential to unlock the development of personalized medicine and microbiome-based therapeutic approaches, improving outcomes and minimizing side effects.
    DOI:  https://doi.org/10.1038/s41467-023-39264-0
  20. FEMS Microbes. 2022 ;3 xtac022
      Secondary bacterial infections increase influenza-related morbidity and mortality, particularly if acquired after 5-7 d from the viral onset. Synergistic host responses and direct pathogen-pathogen interactions are thought to lead to a state of hyperinflammation, but the kinetics of the lung pathology have not yet been detailed, and identifying the contribution of different mechanisms to disease is difficult because these may change over time. To address this gap, we examined host-pathogen and lung pathology dynamics following a secondary bacterial infection initiated at different time points after influenza within a murine model. We then used a mathematical approach to quantify the increased virus dissemination in the lung, coinfection time-dependent bacterial kinetics, and virus-mediated and postbacterial depletion of alveolar macrophages. The data showed that viral loads increase regardless of coinfection timing, which our mathematical model predicted and histomorphometry data confirmed was due to a robust increase in the number of infected cells. Bacterial loads were dependent on the time of coinfection and corresponded to the level of IAV-induced alveolar macrophage depletion. Our mathematical model suggested that the additional depletion of these cells following the bacterial invasion was mediated primarily by the virus. Contrary to current belief, inflammation was not enhanced and did not correlate with neutrophilia. The enhanced disease severity was correlated to inflammation, but this was due to a nonlinearity in this correlation. This study highlights the importance of dissecting nonlinearities during complex infections and demonstrated the increased dissemination of virus within the lung during bacterial coinfection and simultaneous modulation of immune responses during influenza-associated bacterial pneumonia.
    Keywords:  inflammation; influenza; lung injury; mathematical modeling; pneumococcus; viral–bacterial coinfection
    DOI:  https://doi.org/10.1093/femsmc/xtac022
  21. Probiotics Antimicrob Proteins. 2023 Jun 22.
      Probiotic bacteria are known to have ability to tolerate inhospitable conditions experienced during food preparation, food storage, and gastrointestinal tract of consumer. As probiotics are living cells, they are adversely affected by the harsh environment of the carrier matrix as well as low pH, bile salts, oxidative stress, osmotic pressure, and commensal microflora of the host. To overcome the unfavorable environments, many probiotics switch on the cell-mediated protection mechanisms, which helps them to survive, acclimatize and remain operational in the harsh circumstances. In this review, we provide comprehensive understanding on the different stresses experienced by the probiotic when added in carrier food as well as during human gastrointestinal tract transit. Under such situation how these health beneficial bacteria protect themselves by activation of several defense systems and get adapted to the lethal environments.
    Keywords:  GIT; Lactic acid bacteria; Probiotic; Stress
    DOI:  https://doi.org/10.1007/s12602-023-10104-3
  22. Cytotherapy. 2023 Jun 16. pii: S1465-3249(23)00959-3. [Epub ahead of print]
      BACKGROUND/AIMS: Although several studies have demonstrated that mesenchymal stromal cells (MSCs) exhibit beneficial immunomodulatory properties in preclinical models of allergic asthma, effects on airway remodeling have been controversial. Recent evidence has shown that MSCs modify their in vivo immunomodulatory actions depending on the specific inflammatory environment encountered. Accordingly, we assessed whether the therapeutic properties of human mesenchymal stromal cells (hMSCs) could be potentiated by conditioning these cells with serum (hMSC-serum) obtained from patients with asthma and then transplanted in an experimental model of house dust mite (HDM)-induced allergic asthma.METHODS: hMSC and hMSC-serum were administered intratracheally 24 h after the final HDM challenge. hMSC viability and inflammatory mediator production, lung mechanics and histology, bronchoalveolar lavage fluid (BALF) cellularity and biomarker levels, mitochondrial structure and function as well as macrophage polarization and phagocytic capacity were assessed.
    RESULTS: Serum preconditioning led to: (i) increased hMSC apoptosis and expression of transforming growth factor-β, interleukin (IL)-10, tumor necrosis factor-α-stimulated gene 6 protein and indoleamine 2,3-dioxygenase-1; (ii) fission and reduction of the intrinsic respiratory capacity of mitochondria; and (iii) polarization of macrophages to M2 phenotype, which may be associated with a greater percentage of hMSCs phagocytosed by macrophages. Compared with mice receiving hMSCs, administration of hMSC-serum led to further reduction of collagen fiber content, eotaxin levels, total and differential cellularity and increased IL-10 levels in BALF, improving lung mechanics. hMSC-serum promoted greater M2 macrophage polarization as well as macrophage phagocytosis, mainly of apoptotic hMSCs.
    CONCLUSIONS: Serum from patients with asthma led to a greater percentage of hMSCs phagocytosed by macrophages and triggered immunomodulatory responses, resulting in further reductions in both inflammation and remodeling compared with non-preconditioned hMSCs.
    Keywords:  human bone marrow stromal cells; immunomodulation; inflammation; macrophage phagocytosis; macrophage polarization; remodeling
    DOI:  https://doi.org/10.1016/j.jcyt.2023.05.014