Aggeletopoulou Ioanna, Kalafateli Maria, Tsounis Efthymios P, Triantos Christos
Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras, Greece.
Department of Gastroenterology, General Hospital of Patras, Patras, Greece.
Front Med (Lausanne). 2024 Jan 22;11:1307394. doi: 10.3389/fmed.2024.1307394. eCollection 2024.
Interleukin 1β (IL-1β) is a significant mediator of inflammation and tissue damage in IBD. The balance between IL-1β and its endogenous inhibitor-IL-1Ra-, plays a critical role in both initiation and regulation of inflammation. However, the precise role of IL-1β as a causative factor in IBD or simply a consequence of inflammation remains unclear. This review summarizes current knowledge on the molecular and cellular characteristics of IL-1β, describes the existing evidence on the role of this cytokine as a modulator of intestinal homeostasis and an activator of inflammatory responses, and also discusses the role of microRNAs in the regulation of IL-1β-related inflammatory responses in IBD. Current evidence indicates that IL-1β is involved in several aspects during IBD as it greatly contributes to the induction of pro-inflammatory responses through the recruitment and activation of immune cells to the gut mucosa. In parallel, IL-1β is involved in the intestinal barrier disruption and modulates the differentiation and function of T helper (Th) cells by activating the Th17 cell differentiation, known to be involved in the pathogenesis of IBD. Dysbiosis in the gut can also stimulate immune cells to release IL-1β, which, in turn, promotes inflammation. Lastly, increasing evidence pinpoints the central role of miRNAs involvement in IL-1β-related signaling during IBD, particularly in the maintenance of homeostasis within the intestinal epithelium. In conclusion, given the crucial role of IL-1β in the promotion of inflammation and immune responses in IBD, the targeting of this cytokine or its receptors represents a promising therapeutic approach. Further research into the IL-1β-associated post-transcriptional modifications may elucidate the intricate role of this cytokine in immunomodulation.
白细胞介素1β（IL-1β）是炎症性肠病（IBD）中炎症和组织损伤的重要介质。IL-1β与其内源性抑制剂白细胞介素1受体拮抗剂（IL-1Ra）之间的平衡在炎症的起始和调节中均起着关键作用。然而，IL-1β作为IBD致病因素的确切作用，或者仅仅是炎症的一个后果，仍不清楚。本综述总结了目前关于IL-1β分子和细胞特征的知识，描述了关于这种细胞因子作为肠道稳态调节剂和炎症反应激活剂作用的现有证据，并讨论了微小RNA在IBD中IL-1β相关炎症反应调节中的作用。目前的证据表明，IL-1β在IBD过程中涉及多个方面，因为它通过将免疫细胞募集和激活至肠道黏膜，极大地促进了促炎反应的诱导。同时，IL-1β参与肠道屏障破坏，并通过激活已知参与IBD发病机制的辅助性T（Th）细胞17分化来调节Th细胞的分化和功能。肠道微生物群失调也可刺激免疫细胞释放IL-1β，进而促进炎症。最后，越来越多的证据指出微小RNA在IBD期间IL-1β相关信号传导中的核心作用，特别是在维持肠道上皮内稳态方面。总之，鉴于IL-1β在促进IBD炎症和免疫反应中的关键作用，靶向这种细胞因子或其受体代表了一种有前景的治疗方法。对IL-1β相关转录后修饰的进一步研究可能会阐明这种细胞因子在免疫调节中的复杂作用。
