Gut bacteria exacerbates TNBS-induced colitis and kidney injury through oxidative stress

氧化应激 结肠炎 炎症 肠道菌群 医学 免疫学 生物 内科学
作者
Yang Sui,Rui Jiang,Manabu Niimi,Junlin Wang,Yijun Xu,Yingyu Zhang,Zhuheng Shi,Masami Suda,Zhimin Mao,Jianglin Fan,Jian Yao
出处
期刊:Redox biology [Elsevier]
卷期号:72: 103140-103140
标识
DOI:10.1016/j.redox.2024.103140
摘要

Gut microbiota has been implicated in the initiation and progression of various diseases; however, the underlying mechanisms remain elusive and effective therapeutic strategies are scarce. In this study, we investigated the role and mechanisms of gut microbiota in TNBS-induced colitis and its associated kidney injury while evaluating the potential of dietary protein as a therapeutic intervention. The intrarectal administration of TNBS induced colitis in mice, concurrently with kidney damage. Interestingly, this effect was absent when TNBS was administered intraperitoneally, indicating a potential role of gut microbiota. Depletion of gut bacteria with antibiotics significantly attenuated the severity of TNBS-induced inflammation, oxidative damage, and tissue injury in the colon and kidneys. Mechanistic investigations using cultured colon epithelial cells and bone-marrow macrophages unveiled that TNBS induced cell oxidation, inflammation and injury, which was amplified by the bacterial component LPS and mitigated by thiol antioxidants. Importantly, in vivo administration of thiol-rich whey protein entirely prevented TNBS-induced colonic and kidney injury. Our findings suggest that gut bacteria significantly contribute to the initiation and progression of colitis and associated kidney injury, potentially through mechanisms involving LPS-induced exaggeration of oxidative cellular damage. Furthermore, our research highlights the potential of dietary thiol antioxidants as preventive and therapeutic interventions.
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