title: Faecalibacterium prausnitzii upregulates regulatory T cells and anti-inflammatory cytokines in treating TNBS-induced colitis.
abstract: OBJECTIVE
  Faecalibacterium prausnitzii (F. prausnitzii) is a common anaerobic bacteria colonized in the human gut and inflammatory bowel disease (IBD) patients are usually lack of F. prausnitzii. The aims of this study were to evaluate the anti-inflammatory and immunomodulatory capacity of F. prausnitzii by comparing it with Bifidobacterium longum (B. longum) in both cellular and animal experiments.
  
  
  METHODS
  Human peripheral blood mononuclear cells (PBMCs) and 2, 4, 6-trinitrobenzenesulphonic acid (TNBS)-induced colitis rat models were treated with F. prausnitzii, B. longum, F. prausnitzii supernatant or F. prausnitzii medium, respectively. Interleukin (IL)-10, TGF-β1 and IL-12p70 in human PBMCs culture supernatant and rat blood serum were detected. The frequency of CD25(+)Foxp3(+)Treg in human PBMCs, rat PBMCs and rat splenocytes were investigated. Besides, the T-bet, GATA-3, ROR-γt and Foxp3 mRNA in human PBMCs, histopathologic characteristics of the intestinal mucosal and weight loss in the rat models were examined.
  
  
  RESULTS
  F. prausnitzii, B. longum and F. prausnitzii supernatant clearly facilitated the induction of IL-10 and TGF-β1, while induced relatively mild production of IL-12p70 in both cellular and animal models. The F. prausnitzii, B. longum and supernatant differed in their capacity to induce T-bet, GATA-3 and ROR-γt mRNA expression in human PBMCs (both bacterial strains inhibited the expression of ROR-γt while supernatant inhibited the T-bet and GATA-3). However, all of them induced the Foxp3 and Treg production and ameliorated the TNBS-induced colitis. In addition, F. prausnitzii supernatant exhibited the supreme anti-inflammatory capacity.
  
  
  CONCLUSIONS
  F. prausnitzii and its unidentified metabolites in the supernatant are promising candidates in treating IBD, and further research remains necessary to elucidate the safety, efficacy, optimum and mechanism of this bacterium in the clinical practice.
authors: Department of Gastroenterology, Peking University People Hospital, Beijing 100044, China; Department of Gastroenterology, Gulou School of Clinical Medicine, Nanjing Medical University, Nanjing 210008, China.
authors: Xinyun
authors: X
authors: Qiu
authors: Mingming
authors: M
authors: Zhang
authors: Xiaotong
authors: X
authors: Yang
authors: Na
authors: N
authors: Hong
authors: Chenggong
authors: C
authors: Yu
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001644:Bifidobacterium / Q000235:genetics / Q000472:pathogenicity*; D001707:Biopsy, Needle; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics; D016207:Cytokines / Q000187:drug effects / Q000378:metabolism*; D004195:Disease Models, Animal; D006801:Humans; D007150:Immunohistochemistry; D007413:Intestinal Mucosa / Q000187:drug effects / Q000473:pathology; D008297:Male; D019936:Probiotics / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000378:metabolism*; D014302:Trinitrobenzenesulfonic Acid / Q000494:pharmacology*; D015854:Up-Regulation
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D014302:Trinitrobenzenesulfonic Acid
keywords: Bifidobacterium longum; Faecalibacterium prausnitzii; Inflammatory bowel disease; Probiotic; Regulatory T cells