Desulfovibrio vulgaris caused gut inflammation and aggravated DSS-induced colitis in C57BL/6 mice model.

IF 4.3 3区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Gut Pathogens Pub Date : 2024-07-26 DOI:10.1186/s13099-024-00632-w
Guoxin Huang, Yilin Zheng, Ni Zhang, Guohai Huang, Weijin Zhang, Qingnan Li, Xuecong Ren
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Abstract

Background: Sulfate-reducing bacteria (SRB) is a potential pathogen usually detected in patients with gastrointestinal diseases. Hydrogen sulfide (H2S), a metabolic byproduct of SRB, was considered the main causative agent that disrupted the morphology and function of gut epithelial cells. Associated study also showed that flagellin from Desulfovibrio vulgaris (DVF), the representative bacterium of the Desulfovibrio genus, could exacerbate colitis due to the interaction of DVF and LRRC19, leading to the secretion of pro-inflammatory cytokines. However, we still have limited understanding about the change of gut microbiota (GM) composition caused by overgrowth of SRB and its exacerbating effects on colitis.

Results: In this study, we transplanted D. vulgaris into the mice treated with or without DSS, and set a one-week recovery period to investigate the impact of D. vulgaris on the mice model. The outcomes showed that transplanted D. vulgaris into the normal mice could cause the gut inflammation, disrupt gut barrier and reduce the level of short-chain fatty acids (SCFAs). Moreover, D. vulgaris also significantly augmented DSS-induced colitis by exacerbating the damage of gut barrier and the secretion of inflammatory cytokines, for instance, IL-1β, iNOS, and TNF-α. Furthermore, results also showed that D. vulgaris could markedly change GM composition, especially decrease the relative abundance of SCFAs-producing bacteria. Additionally, D. vulgaris significantly stimulated the growth of Akkermansia muciniphila probably via its metabolic byproduct, H2S, in vivo.

Conclusions: Collectively, this study indicated that transplantation of D. vulgaris could cause gut inflammation and aggravate the colitis induced by DSS.

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脱硫弧菌会引起肠道炎症,并加重 C57BL/6 小鼠模型中 DSS 诱导的结肠炎。
背景:硫酸盐还原菌(SRB)是一种潜在的病原体,通常在胃肠道疾病患者体内检测到。硫化氢(H2S)是 SRB 的代谢副产物,被认为是破坏肠道上皮细胞形态和功能的主要致病因子。相关研究还表明,由于 DVF 和 LRRC19 的相互作用,Desulfovibrio vulgaris(DVF)(Desulfovibrio 属的代表细菌)中的鞭毛蛋白可加剧结肠炎,导致促炎细胞因子的分泌。然而,我们对SRB过度生长引起的肠道微生物群(GM)组成变化及其对结肠炎的加重作用的了解仍然有限:在本研究中,我们将 D. vulgaris 移植到接受或不接受 DSS 治疗的小鼠体内,并设定了一周的恢复期,以研究 D. vulgaris 对小鼠模型的影响。结果表明,在正常小鼠体内移植秃头猕猴桃会引起肠道炎症,破坏肠道屏障,降低短链脂肪酸(SCFAs)的水平。此外,D. vulgaris 还能通过加剧肠道屏障的破坏和炎性细胞因子(如 IL-1β、iNOS 和 TNF-α)的分泌,显著增强 DSS 诱导的结肠炎。此外,研究结果还表明,D. vulgaris 还能明显改变基因组的组成,尤其是降低产生 SCFAs 的细菌的相对丰度。此外,D. vulgaris 可能通过其代谢副产物 H2S 显著刺激体内 Akkermansia muciniphila 的生长:总之,这项研究表明,移植 D. vulgaris 可引起肠道炎症,并加重 DSS 诱发的结肠炎。
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来源期刊
Gut Pathogens
Gut Pathogens GASTROENTEROLOGY & HEPATOLOGY-MICROBIOLOGY
CiteScore
7.70
自引率
2.40%
发文量
43
期刊介绍: Gut Pathogens is a fast publishing, inclusive and prominent international journal which recognizes the need for a publishing platform uniquely tailored to reflect the full breadth of research in the biology and medicine of pathogens, commensals and functional microbiota of the gut. The journal publishes basic, clinical and cutting-edge research on all aspects of the above mentioned organisms including probiotic bacteria and yeasts and their products. The scope also covers the related ecology, molecular genetics, physiology and epidemiology of these microbes. The journal actively invites timely reports on the novel aspects of genomics, metagenomics, microbiota profiling and systems biology. Gut Pathogens will also consider, at the discretion of the editors, descriptive studies identifying a new genome sequence of a gut microbe or a series of related microbes (such as those obtained from new hosts, niches, settings, outbreaks and epidemics) and those obtained from single or multiple hosts at one or different time points (chronological evolution).
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