IL-1β is a key mediator of inflammation and tissue damage in inflammatory bowel disease (IBD). It plays a critical role in the initiation and regulation of inflammation by interacting with its endogenous inhibitor, IL-1Ra. While the exact role of IL-1β in IBD remains unclear, current evidence suggests it contributes to the induction of pro-inflammatory responses, intestinal barrier disruption, and the differentiation of T helper (Th) cells, particularly Th17 cells, which are involved in IBD pathogenesis. Dysbiosis in the gut can stimulate immune cells to release IL-1β, which in turn promotes inflammation. Recent studies highlight the role of microRNAs (miRNAs) in regulating IL-1β-related inflammatory responses in IBD, particularly in maintaining intestinal epithelial homeostasis. IL-1β is involved in several aspects of IBD, including the activation of immune cells, the induction of pro-inflammatory responses, and the disruption of the intestinal barrier. Targeting IL-1β or its receptors represents a promising therapeutic approach for IBD. Further research into IL-1β-associated post-transcriptional modifications may elucidate its role in immunomodulation. The NLRP3 inflammasome is a key component in the production of IL-1β and is involved in the regulation of inflammation in IBD. Dysregulation of the NLRP3 inflammasome contributes to excessive inflammation and tissue damage in IBD. Experimental studies have shown that targeting IL-1β or its signaling pathways can reduce colitis severity. IL-1β-targeted therapies, such as IL-1Ra and canakinumab, have shown potential in treating IBD. MiRNAs, such as miR-146a-5p and miR-223, play a regulatory role in IL-1β signaling in IBD, influencing inflammatory responses and maintaining intestinal homeostasis. The role of IL-1β in IBD pathogenesis is complex and involves interactions with the gut microbiota, immune cells, and signaling pathways. Understanding these mechanisms may lead to the development of novel therapeutic strategies for IBD.IL-1β is a key mediator of inflammation and tissue damage in inflammatory bowel disease (IBD). It plays a critical role in the initiation and regulation of inflammation by interacting with its endogenous inhibitor, IL-1Ra. While the exact role of IL-1β in IBD remains unclear, current evidence suggests it contributes to the induction of pro-inflammatory responses, intestinal barrier disruption, and the differentiation of T helper (Th) cells, particularly Th17 cells, which are involved in IBD pathogenesis. Dysbiosis in the gut can stimulate immune cells to release IL-1β, which in turn promotes inflammation. Recent studies highlight the role of microRNAs (miRNAs) in regulating IL-1β-related inflammatory responses in IBD, particularly in maintaining intestinal epithelial homeostasis. IL-1β is involved in several aspects of IBD, including the activation of immune cells, the induction of pro-inflammatory responses, and the disruption of the intestinal barrier. Targeting IL-1β or its receptors represents a promising therapeutic approach for IBD. Further research into IL-1β-associated post-transcriptional modifications may elucidate its role in immunomodulation. The NLRP3 inflammasome is a key component in the production of IL-1β and is involved in the regulation of inflammation in IBD. Dysregulation of the NLRP3 inflammasome contributes to excessive inflammation and tissue damage in IBD. Experimental studies have shown that targeting IL-1β or its signaling pathways can reduce colitis severity. IL-1β-targeted therapies, such as IL-1Ra and canakinumab, have shown potential in treating IBD. MiRNAs, such as miR-146a-5p and miR-223, play a regulatory role in IL-1β signaling in IBD, influencing inflammatory responses and maintaining intestinal homeostasis. The role of IL-1β in IBD pathogenesis is complex and involves interactions with the gut microbiota, immune cells, and signaling pathways. Understanding these mechanisms may lead to the development of novel therapeutic strategies for IBD.