Microbiota-specific Th17 Cells

Wu, Wei; Chen, Feidi; Liu, Zhanju; Cong, Yingzi

doi:10.1097/mib.0000000000000775

Cited by 40 publications

(19 citation statements)

References 102 publications

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“…However, among Th17 cell signature cytokines, IL-17 has been shown to have dual functions during intestinal inflammation: 1) by recruiting myeloid cells (especially neutrophils) to the inflamed intestines (47), and 2) by protecting the intestines from inflammation through the promotion of intestinal IgA production (48) and regulation of epithelial permeability (49). Perhaps not surprisingly, administration of anti-IL-17 antibody has been ineffective in clinic trials for Crohn’s disease (50, 51). IL-22 is crucial in protecting intestinal epithelial barrier function as well as in preventing gut microbiota contact with the host.…”

Section: Discussionmentioning

confidence: 99%

RORγt Represses IL-10 Production in Th17 Cells To Maintain Their Pathogenicity in Inducing Intestinal Inflammation

Sun

Chen

et al. 2019

The Journal of Immunology

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The role of retinoid-related orphan receptor gamma t (RORγt) in Th17 cell differentiation has been well-established, however, how it regulates other T cell lineages is still not clearly understood. We report here that in mice while promoting Th17 cell differentiation, RORγt inhibited IL-10 production by T cells, thereby preserving the pathogenicity of Th17 cells. Treatment with RORγt-specific inhibitor suppressed Th17 cell signature cytokines, but promoted IL-10 production. RORγt inhibitor-treated Th17 cells induce less severe colitis compared to control Th17 cells. Mechanistically, the RORγt inhibitor induced T cell expression of Blimp-1 (encoded by Prdm1). Prdm1−/− T cells produced significant less IL-10 when treated with RORγt inhibitor compared to wild-type (WT) T cells. Furthermore, RORγt inhibitor-treated Prdm1−/− Th17 cells induce more severe colitis compared to RORγt inhibitor-treated WT Th17 cells. Collectively, our studies reveal a novel mechanism by which RORγt drives and maintains pathogenic Th17 cell development by inhibiting IL-10 production.

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Section: Discussionmentioning

confidence: 99%

RORγt Represses IL-10 Production in Th17 Cells To Maintain Their Pathogenicity in Inducing Intestinal Inflammation

Sun

Chen

et al. 2019

The Journal of Immunology

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“…However, in-depth researches on microbiota are very limited. In a recent study, the Yin-Yang theory (Yin and Yang) originating from traditional Chinese medicine has been proposed to explain the complex ecosystem of gut microbiota (Gibson et al, 2014 ; Wu et al, 2016 ; Starkel et al, 2018 ). According to this theory, the Yin-Yang balance is established between the harmful and beneficial microbial cells in the intestine, a process in which two contradictory forces complement and give rise to each other (Cui and Zhang 2018 ).…”

Section: Experiences Of Using Fecal Microbiota In Historymentioning

confidence: 99%

Microbiota transplantation: concept, methodology and strategy for its modernization

Zhang¹,

Cui²,

He³

et al. 2018

Protein Cell

215

192

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Fecal microbiota transplantation (FMT) has become a research focus of biomedicine and clinical medicine in recent years. The clinical response from FMT for different diseases provided evidence for microbiota-host interactions associated with various disorders, including Clostridium difficile infection, inflammatory bowel disease, diabetes mellitus, cancer, liver cirrhosis, gut-brain disease and others. To discuss the experiences of using microbes to treat human diseases from ancient China to current era should be important in moving standardized FMT forward and achieving a better future. Here, we review the changing concept of microbiota transplantation from FMT to selective microbiota transplantation, methodology development of FMT and step-up FMT strategy based on literature and state experts’ perspectives.

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“…5 Sustaining an indigenous microbiota is an integral part of maintaining host health and homeostasis. [5][6][7] Changes in microbiota composition (dysbiosis) or function may cause immune system deregulation and lead to exacerbated inflammatory responses which can contribute to the development of various inflammatory bowel diseases (IBDs) 8,9 and inflammation of the intestine after parasite infection. 10,11 Although the microbiota lodge great variability between individuals at the species level, during IBD and parasite infection, Enterobacteriaceae overgrowth, including E. coli, is commonly found, [10][11][12][13][14] suggesting that this group of microorganisms is involved in the inflammatory response characteristic of IBD.…”

Section: Introductionmentioning

confidence: 99%

Colonization by Enterobacteriaceae is crucial for acute inflammatory responses in murine small intestine via regulation of corticosterone production

et al. 2020

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Although dysbiosis in the gut microbiota is known to be involved in several inflammatory diseases, whether any specific bacterial taxa control host response to inflammatory stimuli is still elusive. Here, we hypothesized that dysbiotic indigenous taxa could be involved in modulating host response to inflammatory triggers. To test this hypothesis, we conducted experiments in germ-free (GF) mice and in mice colonized with dysbiotic taxa identified in conventional (CV) mice subjected to chemotherapy-induced mucositis. First, we report that the absence of microbiota decreased inflammation and damage in the small intestine after administration of the chemotherapeutic agent 5-fluorouracil (5-FU). Also, 5-FU induced a shift in CV microbiota resulting in higher amounts of Enterobacteriaceae, including E. coli, in feces and small intestine and tissue damage. Prevention of Enterobacteriaceae outgrowth by treating mice with ciprofloxacin resulted in diminished 5-FU-induced tissue damage, indicating that this bacterial group is necessary for 5-FU-induced inflammatory response. In addition, monocolonization of germ-free (GF) mice with E. coli led to reversal of the protective phenotype during 5-FU chemotherapy. E. coli monocolonization decreased the basal plasma corticosterone levels and blockade of glucocorticoid receptor in GF mice restored inflammation upon 5-FU treatment. In contrast, treatment of CV mice with ciprofloxacin, that presented reduction of Enterobacteriaceae and E. coli content, induced an increase in corticosterone levels. Altogether, these findings demonstrate that Enterobacteriaceae outgrowth during dysbiosis impacts inflammation and tissue injury in the small intestine. Importantly, indigenous Enterobacteriaceae modulates host production of the anti-inflammatory steroid corticosterone and, consequently, controls inflammatory responsiveness in mice.

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Microbiota-specific Th17 Cells

Cited by 40 publications

References 102 publications

RORγt Represses IL-10 Production in Th17 Cells To Maintain Their Pathogenicity in Inducing Intestinal Inflammation

RORγt Represses IL-10 Production in Th17 Cells To Maintain Their Pathogenicity in Inducing Intestinal Inflammation

Microbiota transplantation: concept, methodology and strategy for its modernization

Colonization by Enterobacteriaceae is crucial for acute inflammatory responses in murine small intestine via regulation of corticosterone production

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