In conclusion, <i>IL-1rn<sup>-/-</sup></i> mice developed spontaneous abnormalities which displayed features associated with IBD, demonstrating a clear role for IL-1 in IBD.
This mini-review will succinctly examine the role of IL-1 family members in IBD, with a special focus on the recently described IL-33 as well as IL-18, and will explore the disease models within which these cytokines have been studied.
We evaluated the effect of DIM on the intestinal permeability of human intestinal cell monolayers and the animal model <i>Caenorhabditis elegans,</i> which were treated with IL-1β and <i>Pseudomonas aeruginosa</i>, respectively, to mimic IBD conditions.
NLRP3 inflammasome has been reported to be associated with inflammatory bowel disease including colitis due to its potential ability to induce IL-1β secretion.
Hispidulin-7-<i>O</i>-neohesperidoside (HN) is flavone diglycoside isolated from the methanolic extract of aerial parts of <i>Cirsium japonicum var</i>. ussuriense.HN concentration-dependently inhibited NO production and considerably downregulated the levels of the proinflammatory cytokines, IL-1β and TNF-α, and the iNOS protein level in LPS-induced RAW 264.7 cells.HN inhibited the production of the chemotactic cytokine, IL-8, in LPS-induced HT-29 cells.HN has potential as an anti-inflammatory agent to prevent and/or treat IBD.
Both of these agents (CpG ODN and herbal extract) showed significant increase in the IFN-γ, IL-2, IL-4, and IL-1 levels in the peripheral blood mononuclear cells (PBMCs) (<i>p</i> < 0.05) of chickens in the treatment groups following IBD infection.Further we found significant reduction in mortality rate in vvIBDV infected chicks treated with either, or in combination, compared with the birds of control group.
Our data unveil an important mechanism by which IL-10 controls IFNγ-secreting CD4<sup>+</sup> T cells in humans and identifies IL-1β as a potential classifier for a subgroup of IBD patients.
Results showed an upregulation of proinflammatory cytokines, including interleukin-1β and interleukin-18, and macrophage infiltration in bursa in response to vvIBDV infection.
In a previous study, we reported that IL-1β decreased mesenteric muscular contractility, consistent with cytokine-mediated changes in contraction present in IBD.
Inflammatory bowel disease (IBD) is associated with enhanced levels of the IL-1 family cytokines IL-1β and IL-18, which are activated by the Nlrp3 inflammasome.
However, while both studies of murine models of gut disease and patients provide data that the main cytokine product generated by this inflammasome, IL-1β, does in fact contribute to inflammation in IBD, there is no evidence that IL-1β plays a decisive or prominent role in "ordinary" patients with IBD (Crohn's disease).
In this study, we show, using Caco-2 cells as a model of intestinal epithelial barrier, that inducing ER stress using a cocktail mixture of pro-inflammatory mediators [TNFα (50ng/ml), MCP1 (50ng/ml), and IL-1β (25ng/ml)] as observed in IBD patients induces ER stress and leads to significant changes in key proteins of the apical (sucrase-isomaltase (SI), dipeptidyl-peptidase (DPPIV), and ezrin) and basolateral (E-cadherin, zonula occludens (ZO-1), and connexin-43) membranes.
In TNBS (2,4,6-trinitrobenzenesulfonic acid)-induced rat colitis model, oral administration of the compounds 5b and 5d ameliorated colitis with significant recovery in altered expressions of E-cadherin, TNF-α and IL-1β expressions, indicating 5b and 5d as potential agents for therapeutics development against IBD.
The aim of the study was to evaluate associations between inflammatory bowel disease (IBD) presentation and variants in NOD2, TLR4, TNF-α, IL-6, IL-1β, and IL-RN genes in order to identify possible environmental factors that may affect IBD occurrence, investigate potential predictors for surgical treatment of IBD, and correlate the presence of granulomas in biopsy specimens with clinical characteristics of Crohn's disease (CD) patients.
In this review, we will discuss the recent advances of novel biologics in clinics and clinical trials, and novel proinflammatory and anti-inflammatory cytokines found in IBD with focusing on IL-12 family and IL-1 family members as well as their relevance to the potential therapy of IBD.
Although the exact aetiology of IBD is unknown, uncontrolled NLRP3 Inflammasome activation has shown to play a major role in the chronic intestinal inflammation and mature IL-1β and IL18 are consistently associated with increased colitis and colitis associated colorectal cancer development.
Other studies have found that mutation of rs1143627 of IL1B (allelic model: OR 2.97; 95% CI 1.74-5.05, P < 0.001) and rs1050152 of OCTN1 (allelic model: OR 1.637, 95% CI 1.078-2.485, P = 0.021) increased the proportion of IBD-associated CRC in the population.
Although antibody responses generated to one variant were potently inhibiting IL-1β, antibody responses induced by the other variant even potentiated the in vivo effects of IL-1β; the latter led to enhanced morbidity in 2 different IL-1β-mediated mouse models, including a model of inflammatory bowel disease and an inflammatory arthritis model.
Members of the IL-1 family regulate the recruitment and activation of effector cells involved in innate and adaptive immunity, but they are also involved in the pathogenesis of chronic disorders, including inflammatory bowel disease, rheumatoid arthritis, and various autoimmune and autoinflammatory diseases.
Canonical NF-κB pathway activation is well studied in IBD and is associated with the rapid, acute production of diverse proinflammatory mediators, such as COX-2, IL-1β, and IL-6.