Treatment and mechanism of fecal microbiota transplantation in mice with experimentally induced ulcerative colitis

Zhang, Leichang; Ma, Xiaofei; Liu, Peng; Ge, Wei; Hu, Li-Xia; Zuo, Zhuang; Xiao, Huirong; Liao, Wu

doi:10.1177/15353702211006044

Cited by 13 publications

(8 citation statements)

References 43 publications

(51 reference statements)

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“…Intestinal microbiota was restored to a compositional pattern close to that of the normal group following treatment with 5‐ASA, accompanied by a reduction in the level of intestinal inflammation. [ 46 ] However, the above results suggested that MBP can better regulate gut microbiota and reverse microbiota dysbiosis after DSS induction than 5‐ASA. Therefore, MBP might be performed by altering the composition of intestinal microorganisms to exhibit anti‐inflammatory and restorative functions of the intestinal barrier.…”

Section: Discussionmentioning

confidence: 97%

Mesona chinensis Benth Polysaccharides Alleviate DSS‐Induced Ulcerative Colitis via Inhibiting of TLR4/MAPK/NF‐κB Signaling Pathways and Modulating Intestinal Microbiota

Shen

Chen

et al. 2022

Molecular Nutrition Food Res

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Scope Ulcerative colitis (UC) is a severe disease of the intestinal tract. To investigate the role of TLR4/Mitogen‐activated protein kinase (MAPK)/Nuclear factor kappa‐B(NF‐κB) pathways and intestinal flora in UC, and the protective mechanisms of Mesona chinensis Benth polysaccharides (MBP), potential therapeutic agents due to their diabetes‐relieving, cancer‐suppressing, and immunomodulatory properties. Methods and results A dextran sulfate sodium (DSS)‐induced mouse colitis model is used for experiments; the histopathology, immunohistochemistry, and Western blotting’s results suggest that MBP can alleviate the colitis symptoms, inhibits the overproduction of TNF‐α, IL‐1β, promote IL‐10, reduces myeloperoxidase activity, and alleviates the inflammatory response probably by inhibiting the activation of TLR4/MAPK/NF‐κB pathways. Furthermore, MBP improvs the ratio of Bcl‐2/BAX, maintains the intestinal integrity by promoting the levels of zonulin occludin‐1 (ZO‐1), occluding and mucin mucin‐2 (MUC‐2), reduces the levels of endotoxin (ET), lipopolysaccharide binding protein (LBP) in serum, and oxidative stress in liver. Moreover, using 16S rRNA Gene Sequencing analysis, MBP regulates gut microbiota by decreasing the abundances of Helicobacter and Prevotella and increasing the abundances of Lactobacillus and Coprococcus, reverses microbiota dysbiosis caused by DSS. Conclusion These findings confirm the anti‐inflammatory effects of MBP, restoration of the intestinal barrier and intestinal flora, and have therapeutic potential to attenuate the development of UC.

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Section: Discussionmentioning

confidence: 97%

Mesona chinensis Benth Polysaccharides Alleviate DSS‐Induced Ulcerative Colitis via Inhibiting of TLR4/MAPK/NF‐κB Signaling Pathways and Modulating Intestinal Microbiota

Shen

Chen

et al. 2022

Molecular Nutrition Food Res

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“…FMT has been proven to be efficacious in treating IBD; however, its mechanism of action remains unclear. Recently, several researchers have focused on studying the (27) found that FMT controlled experimentally induced ulcerative colitis by improving T helper 1 (Th1)/T helper 2 (Th2) and T helper cell 17 (Th17)/regulatory cells (Treg) imbalance through the regulation of the intestinal microbiota. Another study suggested that FMT could increase the abundance of the gut bacteria that produce short-chain fatty acids, which in turn decreased proinflammatory cytokine production by suppressing the nuclear factor-kappa B signaling pathway (28).…”

Section: Discussionmentioning

confidence: 99%

Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis

Qiu¹,

Wu²,

Gao³

et al. 2022

Ann Transl Med

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Background Traditional treatments for inflammatory bowel disease (IBD) have adverse side effects, and patients who receive such treatments have high recurrence rates. Fecal microbiota transplantation (FMT) has become an increasingly popular therapeutic option for patients with IBD. However, the mechanism by which FMT alleviates this disease remains unclear. Methods In this study, a rat model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis was established and used to explore whether the transforming growth factor-beta 1 (TGF-β1)/small mothers against decapentaplegic (Smad) signaling pathway plays a critical role in the FMT alleviation of IBD. Results After the FMT intervention, the disease activity index and histologic scores were significantly decreased. In addition, the TGF-β1 expression level in the FMT group was significantly decreased by approximately 0.72-fold relative to the level in the TNBS colitis group, whereas the Smad3, Smad4, and Smad7 expression levels had increased by approximately 1.21, 1.40, and 1.18 folds, respectively. Similarly, SB431542 inhibited the expression of TGF-β1 and promoted the expression of Smad3, Smad4, and Smad7. Further, the serum levels of the inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were significantly decreased, whereas that of the interferon-gamma (IFN-γ) was not significantly changed after the FMT intervention. Conclusions These results suggest that FMT inhibits the TGF-β1/Smad signaling pathway to attenuate inflammation.

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“…It has been demonstrated that compared with spontaneous recovery without intervention treatment, FMT can help in the rapid recovery of mucosal permeability caused by dysbiosis [69] . In addition, for experimentally induced UC, FMT has been shown to lead to improved intestinal barrier integrity and reduction in colonic inflammation [70] . Therefore, FMT can be used to alleviate, treat, or prevent the occurrence and development of UC.…”

Section: Intestinal Bacteria Are Important Factors For the Development Of Uc And Dysbiosis Further Increases Susceptibility To Ucmentioning

confidence: 99%

MUC2 and related bacterial factors: Therapeutic targets for ulcerative colitis

et al. 2021

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The mucin2 (MUC2) mucus barrier acts as the first barrier that prevents direct contact between intestinal bacteria and colonic epithelial cells. Bacterial factors related to the MUC2 mucus barrier play important roles in the response to changes in dietary patterns, MUC2 mucus barrier dysfunction, contact stimulation with colonic epithelial cells, and mucosal and submucosal inflammation during the occurrence and development of ulcerative colitis (UC). In this review, these underlying mechanisms are summarized and updated, and related interventions for treating UC, such as dietary adjustment, exogenous repair of the mucus barrier, microbiota transplantation and targeted elimination of pathogenic bacteria, are suggested. Such interventions are likely to induce and maintain a long and stable remission period and reduce or even avoid the recurrence of UC. A better mechanistic understanding of the MUC2 mucus barrier and its related bacterial factors may help researchers and clinicians to develop novel approaches for treating UC.

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Treatment and mechanism of fecal microbiota transplantation in mice with experimentally induced ulcerative colitis

Cited by 13 publications

References 43 publications

Mesona chinensis Benth Polysaccharides Alleviate DSS‐Induced Ulcerative Colitis via Inhibiting of TLR4/MAPK/NF‐κB Signaling Pathways and Modulating Intestinal Microbiota

Mesona chinensis Benth Polysaccharides Alleviate DSS‐Induced Ulcerative Colitis via Inhibiting of TLR4/MAPK/NF‐κB Signaling Pathways and Modulating Intestinal Microbiota

Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis

MUC2 and related bacterial factors: Therapeutic targets for ulcerative colitis

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