The Microbiome in Infectious Disease and Inflammation

Honda, Kenya; Littman, Dan R.

doi:10.1146/annurev-immunol-020711-074937

Cited by 706 publications

(606 citation statements)

References 258 publications

(368 reference statements)

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“…2013). Gut microbiota also affect the progression of inflammation (Honda and Littman 2012). The unfavorable combination of inflammation and host genetics promotes development of gut dysbiosis and reduced diversity in the microbial community (Craven et al.…”

Section: Discussionmentioning

confidence: 99%

Mutual reinforcement of pathophysiological host‐microbe interactions in intestinal stasis models

Touw

Ringus

Hubert

et al. 2017

Physiological Reports

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Chronic diseases arise when there is mutual reinforcement of pathophysiological processes that cause an aberrant steady state. Such a sequence of events may underlie chronic constipation, which has been associated with dysbiosis of the gut. In this study we hypothesized that assemblage of microbial communities, directed by slow gastrointestinal transit, affects host function in a way that reinforces constipation and further maintains selection on microbial communities. In our study, we used two models – an opioid‐induced constipation model in mice, and a humanized mouse model where germ‐free mice were colonized with stool from a patient with constipation‐predominant irritable bowel syndrome (IBS‐C) in humans. We examined the impact of pharmacologically (loperamide)‐induced constipation (PIC) and IBS‐C on the structural and functional profile of the gut microbiota. Germ‐free (GF) mice were colonized with microbiota from PIC donor mice and IBS‐C patients to determine how the microbiota affects the host. PIC and IBS‐C promoted changes in the gut microbiota, characterized by increased relative abundance of Bacteroides ovatus and Parabacteroides distasonis in both models. PIC mice exhibited decreased luminal concentrations of butyrate in the cecum and altered metabolic profiles of the gut microbiota. Colonization of GF mice with PIC‐associated mice cecal or human IBS‐C fecal microbiota significantly increased GI transit time when compared to control microbiota recipients. IBS‐C‐associated gut microbiota also impacted colonic contractile properties. Our findings support the concept that constipation is characterized by disease‐associated steady states caused by reinforcement of pathophysiological factors in host‐microbe interactions.

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Section: Discussionmentioning

confidence: 99%

Mutual reinforcement of pathophysiological host‐microbe interactions in intestinal stasis models

Touw

Ringus

Hubert

et al. 2017

Physiological Reports

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“…The composition of the intestinal microbiota regulates the balance between Th17 and Treg cells in the lamina propria and influences intestinal homeostasis (Honda and Littman 2012). Treg-cell numbers are increased in the colonic lamina propria compared with other organs, and these numbers are reduced in germ-free or antibiotics-treated mice, suggesting that the nature of the microbiota affects colonic pTregcell differentiation (Atarashi et al 2011;Honda and Littman 2012).…”

Section: Microbiomementioning

confidence: 99%

“…Treg-cell numbers are increased in the colonic lamina propria compared with other organs, and these numbers are reduced in germ-free or antibiotics-treated mice, suggesting that the nature of the microbiota affects colonic pTregcell differentiation (Atarashi et al 2011;Honda and Littman 2012). A cocktail of 17 strains of bacteria, belonging to the clusters of Clostridium species, isolated from the stool of a healthy human provided bacterial antigens and a TGFb-rich environment to support the expansion of Treg cells in germ-free mice (Atarashi et al 2013).…”

Section: Microbiomementioning

confidence: 99%

Regulation of the Immune Response by TGF-β: From Conception to Autoimmunity and Infection

Sanjabi

2017

Cold Spring Harb Perspect Biol

451

306

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Transforming growth factor b (TGF-b) is a pleiotropic cytokine involved in both suppressive and inflammatory immune responses. After 30 years of intense study, we have only begun to elucidate how TGF-b alters immunity under various conditions. Under steady-state conditions, TGF-b regulates thymic T-cell selection and maintains homeostasis of the naïve T-cell pool. TGF-b inhibits cytotoxic T lymphocyte (CTL), Th1-, and Th2-cell differentiation while promoting peripheral ( p)Treg-, Th17-, Th9-, and Tfh-cell generation, and T-cell tissue residence in response to immune challenges. Similarly, TGF-b controls the proliferation, survival, activation, and differentiation of B cells, as well as the development and functions of innate cells, including natural killer (NK) cells, macrophages, dendritic cells, and granulocytes. Collectively, TGF-b plays a pivotal role in maintaining peripheral tolerance against self-and innocuous antigens, such as food, commensal bacteria, and fetal alloantigens, and in controlling immune responses to pathogens.

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“…At the mucosa the microbiota is in constant, close, contact with both innate and adaptive immune cells 20, 21, 22. This promotes the development and maturation of the mucosal immune system 20, 22. The resulting agglomeration of immune cells and structures helps to manage and contain the microbiota at the mucosa 23, 24.…”

Section: Introductionmentioning

confidence: 99%

The regulation of host defences to infection by the microbiota

Brown

Clarke

2016

Immunology

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SummaryThe skin and mucosal epithelia of humans and other mammals are permanently colonized by large microbial communities (the microbiota). Due to this life‐long association with the microbiota, these microbes have an extensive influence over the physiology of their host organism. It is now becoming apparent that nearly all tissues and organ systems, whether in direct contact with the microbiota or in deeper host sites, are under microbial influence. The immune system is perhaps the most profoundly affected, with the microbiota programming both its innate and adaptive arms. The regulation of immunity by the microbiota helps to protect the host against intestinal and extra‐intestinal infection by many classes of pathogen. In this review, we will discuss the experimental evidence supporting a role for the microbiota in regulating host defences to extra‐intestinal infection, draw together common mechanistic themes, including the central role of pattern recognition receptors, and outline outstanding questions that need to be answered.

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The Microbiome in Infectious Disease and Inflammation

Cited by 706 publications

References 258 publications

Mutual reinforcement of pathophysiological host‐microbe interactions in intestinal stasis models

Mutual reinforcement of pathophysiological host‐microbe interactions in intestinal stasis models

Regulation of the Immune Response by TGF-β: From Conception to Autoimmunity and Infection

The regulation of host defences to infection by the microbiota

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