Regulation of innate and adaptive immunity by the commensal microbiota

Infectious Diseases Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center, Immunology Program, Sloan-Kettering Institute, New York, NY 10065, United States.
Current opinion in immunology (Impact Factor: 7.48). 04/2011; 23(3):353-60. DOI: 10.1016/j.coi.2011.03.001
Source: PubMed


The microbial communities that inhabit the intestinal tract are essential for mammalian health. Communication between the microbiota and the host establishes and maintains immune homeostasis, enabling protective immune responses against pathogens while preventing adverse inflammatory responses to harmless commensal microbes. Specific bacteria, such as segmented filamentous bacteria, Clostridium species, and Bacteroides fragilis, are key contributors to immune homeostasis in the gut. The cellular and molecular interactions between intestinal microbes and the immune system are rapidly being elucidated. Here, we review advances in our understanding of the microbial populations that shape the mucosal immune system and create a protective defense that prevents infection while tolerating friendly commensals.

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    • "However, recolonizing germ-free mice (GF) with species-specific microbiota restored the intestinal immune compartment and reduced Salmonella fecal CFUs 4 days post infection (Chung et al., 2012). Commensal-induced Th17 cells also contribute to pathogen defense by producing IL-17 and IL-22, which promote antibody class switching in B cells, induce anti-microbial peptides and contribute to neutrophil recruitment (Jarchum and Pamer, 2011; Littman and Pamer, 2011; Maynard et al., 2012). The microbiota also sends signals to immune cells in the intestinal compartment through pattern recognition receptors such as TLRs. "
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    ABSTRACT: The intestinal commensal microbiota is essential for many host physiological processes, but its impact on infectious diseases is poorly understood. Here we investigate the influence of the gut microbiota during oral Salmonella infection. We report a higher bacterial burden in mesenteric lymph nodes (MLN) of intragastrically infected germ-free (GF) mice compared to conventionally-raised (CONV-R) animals, despite similar inflammatory phagocyte recruitment. Salmonella penetration into the lamina propria of the small intestine and splenic bacterial burden were not altered in the absence of the microbiota. Intragastrically infected GF mice also displayed a higher frequency of IFN-γ-producing NK, NKT, CD4+ and CD8+ T cells in the MLN despite IL-12 levels similar to infected CONV-R mice. However, infecting mice intraperitoneally abrogated the difference in MLN bacterial load and IFN-γ-producing cells observed in intragastrically-infected animals. Moreover, mice treated with antibiotics (ABX) and intragastrically infected with Salmonella had a greater bacterial burden and frequency of IFN-γ-producing cells in the MLN. In ABX mice the number of Salmonella correlated with the frequency of IFN-γ-producing lymphocytes in the MLN, while no such correlation was observed in the MLN of infected GF mice. Overall, the data show that the lack of the microbiota influences pathogen colonization of the MLN, and the increased IFN-γ in the MLN of infected GF mice is not only due to the absence of commensals at the time of infection but the lack of immune signals provided by the microbiota from birth.
    Full-text · Article · Dec 2015 · Frontiers in Cellular and Infection Microbiology
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    • "Intestinal microorganisms are crucially involved in the induction and modulation of mucosal tolerance (Noverr and Huffnagle, 2004; Sanz and De Palma, 2009; Peterson and Cardona, 2010; Tlaskalová-Hogenová et al., 2011; Huang et al., 2013; Ma et al., 2015). Alterations in mucosal tolerance induced by imbalanced gut microflora may lead to acute or chronic inflammation (Sanz and De Palma, 2009; Chow et al., 2010; Lee and Mazmanian, 2010; Jarchum and Pamer, 2011; Swiatczak and Rescigno, 2012; Magrone and Jirillo, 2013; Chistiakov et al., 2015). The effects of imbalanced microbiota are not restricted by gastrointestinal abnormalities but could have systemic impact on immunity (Noverr and Huffnagle, 2004; Huang et al., 2013; Ma et al., 2015). "
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    ABSTRACT: Inflammation and metabolic abnormalities are linked to each other. At present, pathogenic inflammatory response was recognized as a major player in metabolic diseases. In humans, intestinal microflora could significantly influence the development of metabolic diseases including atherosclerosis. Commensal bacteria were shown to activate inflammatory pathways through altering lipid metabolism in adipocytes, macrophages, and vascular cells, inducing insulin resistance, and producing trimethylamine-N-oxide. However, gut microbiota could also play the atheroprotective role associated with anthocyanin metabolism and administration of probiotics and their components. Here, we review the mechanisms by which the gut microbiota may influence atherogenesis.
    Full-text · Article · Jun 2015 · Frontiers in Microbiology
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    • "One aspect of TB infection that remains largely unexplored is the role of the resident microbiota (the microorganisms that collectively live on or in mammals). It is now well recognized that the gastrointestinal microbiota maintain a complex, reciprocal relationship with the host immune system [4], [5], [6], [7]. Moreover, differences in fecal microbiota composition and functional potential have been identified in individuals with various disease states when compared to healthy individuals, including inflammatory bowel disease, arthritis, type 2 diabetes, and asthma [8], [9], [10]. "
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    ABSTRACT: Mycobacterium tuberculosis is an important human pathogen, and yet diagnosis remains challenging. Little research has focused on the impact of M. tuberculosis on the gut microbiota, despite the significant immunological and homeostatic functions of the gastrointestinal tract. To determine the effect of M. tuberculosis infection on the gut microbiota, we followed mice from M. tuberculosis aerosol infection until death, using 16S rRNA sequencing. We saw a rapid change in the gut microbiota in response to infection, with all mice showing a loss and then recovery of microbial community diversity, and found that pre-infection samples clustered separately from post-infection samples, using ecological beta-diversity measures. The effect on the fecal microbiota was observed as rapidly as six days following lung infection. Analysis of additional mice infected by a different M. tuberculosis strain corroborated these results, together demonstrating that the mouse gut microbiota significantly changes with M. tuberculosis infection.
    Full-text · Article · May 2014 · PLoS ONE
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