Qiu Jinlang, Wu Caixian, Gao Qianyu, Li Sheng, Li Yuhua
Department of Clinical Laboratory, Fuzhou Traditional Chinese Medicine Hospital, Fuzhou, China.
Department of Anus-Intestines, The Second Affiliated Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, China.
Ann Transl Med. 2022 Aug;10(15):825. doi: 10.21037/atm-22-3227.
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.
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.
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.
These results suggest that FMT inhibits the TGF-β1/Smad signaling pathway to attenuate inflammation.
炎症性肠病(IBD)的传统治疗方法有不良副作用,接受此类治疗的患者复发率高。粪便微生物群移植(FMT)已成为IBD患者越来越受欢迎的治疗选择。然而,FMT缓解该病的机制仍不清楚。
在本研究中,建立了2,4,6-三硝基苯磺酸(TNBS)诱导的大鼠结肠炎模型,用于探究转化生长因子-β1(TGF-β1)/抗五聚体小母亲(Smad)信号通路在FMT缓解IBD中是否起关键作用。
FMT干预后,疾病活动指数和组织学评分显著降低。此外,FMT组中TGF-β1的表达水平相对于TNBS结肠炎组显著降低了约0.72倍,而Smad3、Smad4和Smad7的表达水平分别增加了约1.21、1.40和1.18倍。同样,SB431542抑制TGF-β1的表达并促进Smad3、Smad4和Smad7的表达。此外,FMT干预后,炎症细胞因子肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的血清水平显著降低,而干扰素-γ(IFN-γ)的血清水平没有显著变化。
这些结果表明,FMT通过抑制TGF-β1/Smad信号通路减轻炎症。