Enterobacter ludwigii protects DSS-induced colitis through choline-mediated immune tolerance

Li, Qianqian; Sun, Xuan; Kobayashi, Yu; Lv, Junqiang; Miao, Chunhui; Yang, Jianming; Wang, Song; Fu, Zheng; Sun, Yi; Zhang, Hong; Zhang, Zhisong; Keller, Evan T.; Yao, Zhi; Wang, Quan

doi:10.1016/j.celrep.2022.111308

Cited by 17 publications

(24 citation statements)

References 55 publications

(60 reference statements)

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“…37 To investigate these factors, a colitis mouse model was constructed in this study using DSS challenge, which is a common approach in colitis research. [38][39][40] The inflammatory process and immunopathology observed in this mouse model are similar with those seen in human IBDs, making it a suitable model for our study. Compared with the mice in DSS group, addition of daphnetin treatment substantially reduced the severity of UC symptoms, including bodyweight loss, colon length shortening, DAI score increase, and epithelial damage.…”

Section: Discussionmentioning

confidence: 73%

“…Although the exact mechanisms underlying the development of IBDs are not yet fully understood, existing evidence suggests that sustained inflammation and injury are implicated in their pathogenesis 37 . To investigate these factors, a colitis mouse model was constructed in this study using DSS challenge, which is a common approach in colitis research 38–40 . The inflammatory process and immunopathology observed in this mouse model are similar with those seen in human IBDs, making it a suitable model for our study.…”

Section: Discussionmentioning

confidence: 97%

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Daphnetin attenuates intestinal inflammation, oxidative stress, and apoptosis in ulcerative colitis via inhibiting REG3A‐dependent JAK2/STAT3 signaling pathway

Liu

2023

Environmental Toxicology

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Daphnetin is a natural coumarin compound with anti‐inflammatory, anti‐oxidant, and anti‐apoptotic effects, which has been previously demonstrated to ameliorate DSS‐induced ulcerative colitis (UC). However, the molecular mechanism involved in the daphnetin‐mediated pathological process of UC remains unclarified. The current study used DSS‐induced mice and LPS‐challenged Caco‐2 cells as UC models. Bodyweight, disease activity index (DAI) score, and colon length were used to evaluate the severity of colitis. The histological changes in colon tissues were observed using H&E and PAS staining. Protein levels were detected by western blot. The malondialdehyde (MDA) and superoxide dismutase (SOD) activities were used to assess oxidative stress. Inflammatory responses were evaluated by detecting the levels of inflammatory cytokines (IFN‐r, IL‐1β, IL‐6, and TNF‐α) using flow cytometry. CCK‐8 and TUNEL assay were employed to determine cell growth and cell death, respectively. The results showed that daphnetin could ameliorate the severity of colitis and attenuate the damage to intestinal structure in DSS‐induced mice. Compared with the DSS group, the expression of ZO‐1, occludin, and anti‐apoptotic protein (BCL‐2) was increased while the level of pro‐apoptotic proteins (Bax and cleaved caspase 3) was decreased in DSS + daphnetin group. The activity of MDA and SOD, as well as the levels of inflammatory cytokines were substantially suppressed by daphnetin. In consistency, in vitro assays indicated that daphnetin protected Caco‐2 cells from LPS‐stimulated viability impairment, apoptosis, oxidative stress, and inflammation. Furthermore, daphnetin suppressed the activity of JAK2/STAT signaling in LPS‐induced Caco‐2 cells in a REG3A‐dependent manner. REG3A overexpression abated the ameliorative effects of daphnetin while JAK2/STAT signaling inhibition functioned synergically with daphnetin in LPS‐stimulated Caco‐2 cells. Collectively, this study deepened the understanding of the therapeutic effects of daphnetin on UC and uncovered for the first time that daphnetin functioned through REG3A‐activated JAK2/STAT3 signaling in UC, which may provide novel insights for the treatment of UC.

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Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 97%

Daphnetin attenuates intestinal inflammation, oxidative stress, and apoptosis in ulcerative colitis via inhibiting REG3A‐dependent JAK2/STAT3 signaling pathway

Liu

2023

Environmental Toxicology

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“…Furthermore, according to a recent study by Wang et al, Enterobacter ludwigii isolated from metronidazole-treated mouse feces could enhance DCs and promote Tregs differentiation through its metabolite choline and its receptor α7 nicotinic acetylcholine receptor (α7nAChR)mediated upregulation of retinoic acid (RA) and TGF-β, thereby increasing the CD103+ DC/Treg-dependent tolerance response and ultimately reducing the susceptibility of mice to DSS-induced colitis. Thus, this study provides a potential therapeutic approach for IBD (Li et al, 2022).…”

Section: Bacteria Species and Functional Pathways That Are Potentiall...mentioning

confidence: 90%

New insights into bacterial mechanisms and potential intestinal epithelial cell therapeutic targets of inflammatory bowel disease

Liang

Wang

et al. 2022

Front. Microbiol.

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The global incidence of inflammatory bowel disease (IBD) has increased rapidly in recent years, but its exact etiology remains unclear. In the past decade, IBD has been reported to be associated with dysbiosis of gut microbiota. Although not yet proven to be a cause or consequence of IBD, the common hypothesis is that at least some alterations in the microbiome are protective or pathogenic. Furthermore, intestinal epithelial cells (IECs) serve as a protective physical barrier for gut microbiota, essential for maintaining intestinal homeostasis and actively contributes to the mucosal immune system. Thus, dysregulation within the intestinal epithelium increases intestinal permeability, promotes the entry of bacteria, toxins, and macromolecules, and disrupts intestinal immune homeostasis, all of which are associated with the clinical course of IBD. This article presents a selective overview of recent studies on bacterial mechanisms that may be protective or promotive of IBD in biological models. Moreover, we summarize and discuss the recent discovery of key modulators and signaling pathways in the IECs that could serve as potential IBD therapeutic targets. Understanding the role of the IECs in the pathogenesis of IBD may help improve the understanding of the inflammatory process and the identification of potential therapeutic targets to help ameliorate this increasingly common disease.

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“…The oral administration of L. rhamnosus GG reduced inflammatory cytokine levels and improved colonic histology scores, which prevented colitis relapse in rats during antibiotic treatment [ 56 ]. Additionally, a study using mouse models of colitis showed that Enterobacter ludwigii was effective in alleviating the symptoms of colitis [ 57 ]. In a dextran sulfate sodium (DSS)-induced colitis mouse model, compared with that of other antibiotic treatments, metronidazole had the best effect in reducing colitis, which was related to an increase in the abundance of the gut microbiota species E. ludwigii .…”

Section: Effect Of Probiotics Prebiotics and Symbiotics On Ibdmentioning

confidence: 99%

“…In a dextran sulfate sodium (DSS)-induced colitis mouse model, compared with that of other antibiotic treatments, metronidazole had the best effect in reducing colitis, which was related to an increase in the abundance of the gut microbiota species E. ludwigii . The administration of E. ludwigii induced Treg differentiation via metabolites from E. ludwigii and increased the immune tolerance response, which reduced the susceptibility to DSS-induced colitis in mice [ 57 ].…”

Section: Effect Of Probiotics Prebiotics and Symbiotics On Ibdmentioning

confidence: 99%

Inflammatory Bowel Diseases and Gut Microbiota

Haneishi

Furuya

Hasegawa

et al. 2023

IJMS

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Inflammatory bowel disease (IBD) is an inflammatory disease of the gastrointestinal tract, the incidence of which has rapidly increased worldwide, especially in developing and Western countries. Recent research has suggested that genetic factors, the environment, microbiota, and immune responses are involved in the pathogenesis; however, the underlying causes of IBD are unclear. Recently, gut microbiota dysbiosis, especially a decrease in the abundance and diversity of specific genera, has been suggested as a trigger for IBD-initiating events. Improving the gut microbiota and identifying the specific bacterial species in IBD are essential for understanding the pathogenesis and treatment of IBD and autoimmune diseases. Here, we review the different aspects of the role played by gut microbiota in the pathogenesis of IBD and provide a theoretical basis for modulating gut microbiota through probiotics, fecal microbiota transplantation, and microbial metabolites.

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Enterobacter ludwigii protects DSS-induced colitis through choline-mediated immune tolerance

Cited by 17 publications

References 55 publications

Daphnetin attenuates intestinal inflammation, oxidative stress, and apoptosis in ulcerative colitis via inhibiting REG3A‐dependent JAK2/STAT3 signaling pathway

Daphnetin attenuates intestinal inflammation, oxidative stress, and apoptosis in ulcerative colitis via inhibiting REG3A‐dependent JAK2/STAT3 signaling pathway

New insights into bacterial mechanisms and potential intestinal epithelial cell therapeutic targets of inflammatory bowel disease

Inflammatory Bowel Diseases and Gut Microbiota

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