
-   Intestine tissues from patients with ulcerative colitis and mice with colitis have increased levels of IL1B mRNA and MIR200C-3p, which reduces expression of occludin by enterocytes and thereby increases tight junction (TJ) permeability [PMID: 32569770].
-   The C. difficile-infected (CDI) RR mice induced a higher magnitude of CXCR2 upregulation and had more IL-1beta; IL-1beta neutralization reduced CXCR2 expression on bone marrow and blood neutrophils and their subsequent accrual to colonic tissue. These data indicate that IL-1beta is a key molecular mediator that communicates between gastro-intestinal tract (i.e. site of CDI) and bone marrow (i.e. primary neutrophil reservoir) and regulates the intensity of CDI-induced tissue neutrophilia by modulating CXCR2 expression [PMID: 33718269].
-   IL-1 beta interacts with FGF-2 to amplify the proliferation of primary rat aortic smooth muscle cells, an effect that may be important in vascular smooth muscle cell proliferation following vascular injury [PMID: 7544359].
-   Interleukin-1 beta (IL-1beta) in synergy with tumour necrosis factor alpha (TNFalpha) and interferon gamma (IFNgamma) is cytotoxic to pancreatic beta cells. TNFalpha and IFNgamma were found to synergistically increase mitogen-activated protein kinase activity induced by IL-1beta in rat pancreatic islets of Langerhans [PMID: 11126408].

## Summary

IL1B encodes interleukin-1 beta (IL-1beta), a potent pro-inflammatory cytokine that mediates diverse cellular activities, including cell proliferation, differentiation, and apoptosis [CS: 10]. It is produced by activated macrophages and has a crucial role in the inflammatory response [CS: 10]. In the context of colon diseases and toxicities, IL1B expression is often upregulated [CS: 8].

For instance, in CC and obesity, there is a notable increase in IL1B mRNA levels in visceral adipose tissue [CS: 7]. This upregulation can be seen as the body's response to the inflammatory conditions prevalent in these diseases [CS: 8]. IL-1beta aids in the recruitment and activation of immune cells, including neutrophils and T-cells [CS: 9]. This action fosters an environment conducive to tumor progression or exacerbates inflammation in obesity [CS: 7]. Similarly, in ulcerative colitis, the increased levels of IL1B mRNA lead to higher IL-1beta production, intensifying inflammation [CS: 8]. This heightened inflammation is marked by the disruption of tight junction integrity, primarily due to IL-1beta's role in decreasing occludin expression by enterocytes [CS: 7]. This action aligns with IL-1beta's broader function in promoting inflammation and immune cell recruitment, which, although intended to counteract threats, can unintentionally amplify tissue damage and disease symptoms [CS: 9].
