However, more recent evidence from various autoimmune diseases (e.g., inflammatory bowel disease, rheumatoid arthritis) has shown that the IL-6 activity is more complex with important effects also on tissue homeostasis, regeneration, and metabolism.
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.
The aim of this study was to assess the relationship between polymorphisms involving five cytokine genes (TNF-alpha, TGF-beta, IL-10, IL-6, and IFN-gamma), and IBD susceptibility and disease phenotype.
The aim of the study was to evaluate bone mineral density (BMD) by densitometry and the concentration of interleukin 6, osteoprotegerin (OPG) and sRANKL protein (sRANKL) by ELISA in patients with IBD in relation to the control group; to assess the relationship between IL-6, OPG, sRANKL and BMD; and to assess the impact of disease duration and number hospitalization on BMD.
Evidence of active cytomegalovirus infection and increased production of IL-6 in tissue specimens obtained from patients with inflammatory bowel diseases.
We used recombinant sgp130Fc protein and recently generated transgenic mice expressing high levels of sgp130Fc to discriminate between classic and trans-signaling in vivo, and demonstrated that IL-6 trans-signaling is critically involved in generation and maintenance of several inflammatory and autoimmune diseases including chronic inflammatory bowel disease, rheumatoid arthritis, peritonitis and asthma, as well as inflammation-induced colon cancer.
The interleukin-6 (IL-6)/STAT3 signaling regulates survival and proliferation of intestinal epithelial cells and plays an important role in the pathogenesis of inflammatory bowel disease and colorectal cancer.
T helper 17 (Th17)-cell differentiation triggered by interleukin-6 (IL-6) via STAT3 activation promotes inflammation in inflammatory bowel disease (IBD) patients.
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.
These results confirmed that the Th17 cell subset was specifically activated in PP and demonstrated that IL‑6 is required in Th17 cell activation, which are important to the clinical treatment of IBD.
Gastrointestinal perforation may be a specific concern for agents directed at interleukin-6 pathways, and some reports have raised the question of whether interleukin-17 inhibition may elevate inflammatory bowel disease risk.
Cytokine expression in intestinal mucosal biopsies. In situ hybridisation of the mRNA for interleukin-1 beta, interleukin-6 and tumour necrosis factor-alpha in inflammatory bowel disease.
Comparing the change of the variables indicated a significant decrease in fecal calprotectin (P < 0.001), Mayo score (P < 0.001), ESR (P < 0.001), INF-γ (P < 0.001), IL-6 (P < 0.001), waist circumference (P = 0.02), Diastolic Blood Pressure (DBP) (P < 0.001), and Systolic Blood Pressure (SBP) (P < 0.001) and a significant increase in TGF-β (P < 0.001) and Inflammatory Bowel Disease Questionnaire-Short form (IBDQ-9) score (P < 0.001) in the GF and FO groups compared to the control.
Our data define a new function of IL-6 and suggest that caution should be exercised when targeting IL-6 in IBD patients, particularly those with defects in IL-10 signaling.
Taken together, our data identify IRF4 as a key regulator of mucosal IL-6 production in T cell-dependent experimental colitis and suggest that IRF4 might provide a therapeutic target for IBDs.
The aim of the study was to describe the levels of circulating monocyte/macrophage pro-inflammatory cytokines (TNF-alpha, IL-1beta IL-6, and IL-8) and an anti-inflammatory cytokine (IL-10) in inflammatory bowel disease (IBD) and colorectal cancer (CRC) patients and healthy controls.
Down-regulation of intestinal trefoil factor TFF3 due to transcriptional repression by IL1beta through NF-kappaB as well as by IL6 through C/EBPbeta activation in vitro may reflect the situation in vivo and may contribute to ulceration and decreased wound healing during inflammatory bowel disease.
Elevated expression of Foxp3, IL-17a, IL-1beta, and IL-6 was observed in the mucosa of IBD patients, while TGF-beta was only elevated in ulcerative colitis.