背景:硫酸盐还原菌(SRB)是通常在胃肠道疾病患者中检测到的潜在病原体。硫化氢(H2S),SRB的代谢副产物,被认为是破坏肠上皮细胞形态和功能的主要病原体。相关研究还表明,来自寻常脱硫弧菌(DVF)的鞭毛蛋白,脱硫弧菌属的代表性细菌,可能由于DVF和LRRC19的相互作用而加剧结肠炎,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菌群(GM)组成变化及其对结肠炎的加重作用的认识仍然有限.
结果:在这项研究中,我们将普通D.vulgaris移植到用或不用DSS处理的小鼠中,并设定一个为期一周的恢复期来研究普通D.结果显示,将普通D.vulgaris移植到正常小鼠体内会引起肠道炎症,破坏肠道屏障并降低短链脂肪酸(SCFA)的水平。此外,D.vulgaris也显著增加DSS诱导的结肠炎,通过加剧肠道屏障的损伤和炎症细胞因子的分泌,例如,IL-1β,iNOS,和TNF-α。此外,结果还表明,普通D。可以显着改变转基因成分,特别是降低了产生SCFAs的细菌的相对丰度。此外,D.vulgaris显着刺激了Akkermansiamuciniphila的生长,可能是通过其代谢副产物,H2S,在体内。
结论:总的来说,本研究表明,普通D.vulgaris移植可引起肠道炎症,加重DSS诱导的结肠炎。
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.