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鞘氨醇-1-磷酸的功能性拮抗剂FTY720会损害肠道屏障功能。

The functional antagonist of sphingosine-1-phosphate, FTY720, impairs gut barrier function.

作者信息

Sikdar Sohini, Mitra Debmalya, Das Oishika, Bhaumik Moumita, Dutta Shanta

机构信息

Division of Immunology , ICMR-National Institute for Research in Bacterial Infections (NIRBI), Kolkata, India.

Center of Radiological Research, Columbia University Irving Medical Center, New York, NY, United States.

出版信息

Front Pharmacol. 2024 Aug 19;15:1407228. doi: 10.3389/fphar.2024.1407228. eCollection 2024.

Abstract

FTY720 or fingolimod is a known functional antagonist of sphingosine-1-phosphate (S1P), and it is effective in treating multiple sclerosis and preventing inflammatory bowel disease (IBD). Evidence shows that its use in mice can increase the susceptibility to mucosal infections. Despite the significant contribution of S1P to barrier function, the effect of the administration of FTY720 on the mucosal barrier has never been investigated. In this study, we looked into how FTY720 therapy affected the function of the gut barrier susceptibility. Administration of FTY720 to C57BL/6 mice enhances the claudin-2 expression and reduces the expression of claudin-4 and occludin, as studied by qPCR, Western blot, and immunofluorescence. FTY720 inhibits the Akt-mTOR pathway to decrease occludin and claudin-4 expression and increase claudin-2 expression. FTY720 treatment induced increased colonic inflammation, with notably greater immune cell infiltration, colon histopathology, and increased production of TNF-α, IFN-γ, CXCL-1, and CXCL-2 than that in control mice. Taking into account the close association of "the leaky gut" and gut dysbiosis among the major diseases, we therefore can infer that the vigilance of gut pathology should be maintained, where FTY720 is used as a treatment option.

摘要

FTY720(即芬戈莫德)是一种已知的鞘氨醇-1-磷酸(S1P)功能性拮抗剂,对治疗多发性硬化症和预防炎症性肠病(IBD)有效。有证据表明,在小鼠中使用它会增加黏膜感染的易感性。尽管S1P对屏障功能有重要作用,但FTY720给药对黏膜屏障的影响从未被研究过。在本研究中,我们探究了FTY720治疗如何影响肠道屏障易感性的功能。通过qPCR、蛋白质免疫印迹和免疫荧光研究发现,给C57BL/6小鼠施用FTY720可增强紧密连接蛋白-2(claudin-2)的表达,并降低紧密连接蛋白-4(claudin-4)和闭合蛋白(occludin)的表达。FTY720抑制Akt-雷帕霉素靶蛋白(mTOR)信号通路,以降低occludin和claudin-4的表达,并增加claudin-2的表达。与对照小鼠相比,FTY720治疗导致结肠炎症增加,免疫细胞浸润、结肠组织病理学显著加重,肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)、CXC趋化因子配体1(CXCL-1)和CXC趋化因子配体2(CXCL-2)的产生增加。鉴于“肠道渗漏(the leaky gut)”与主要疾病中的肠道菌群失调密切相关,因此我们可以推断,在将FTY720用作治疗选择时,应保持对肠道病理学的警惕。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ec/11366638/388ca15a94e4/fphar-15-1407228-g001.jpg

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