CXCL16 is a surrogate marker of inflammatory bowel disease.

OBJECTIVE: Impaired barrier function of the gut and inadequate immunological response to intestinal pathogens are the cornerstones in the pathogenesis of inflammatory bowel disease (IBD). CXCL16 is a protein which shares pattern recognition receptor functions, relevant for adhesion and phagocytosis of bacterial products, with the properties of an adhesion molecule and inflammatory chemokine. The relevance of CXCL16 in IBD has so far been elusive. This objective of this study was to determine the association between CXCL16 and IBD. MATERIAL AND METHODS: Soluble CXCL16 (sol-CXCL16) serum levels in a cohort of 239 patients with Crohn's disease were measured, 114 patients with ulcerative colitis and 144 controls. RESULTS: In a univariate analysis, sol-CXCL16 was found to be markedly increased in patients with Crohn's disease or ulcerative colitis compared with that in controls (p < 0.001). This was significantly associated with an increase of the inflammatory marker C-reactive protein (CRP) (p < 0.01). In the multivariate analysis (adjusted for age, gender, body mass index (BMI), white blood cell (WBC) count, resistin and CRP) sol-CXCL16 was associated with Crohn's disease above versus below the median (OR 10.53 (3.97-27.78) p < 0.001) and ulcerative colitis (OR 3.46 (1.40-8.55) p < 0.01). CONCLUSION: Our findings suggest that CXCL16 may play a pro-inflammatory role in IBD, particularly Crohn's disease.

Resistin is an inflammatory marker of inflammatory bowel disease in humans.

OBJECTIVES: Resistin, a recently discovered adipokine, has been shown to be associated with inflammatory conditions such as insulin resistance, obesity, atherosclerosis and rheumatoid arthritis. We therefore hypothesized that (i) resistin levels may be elevated in patients with inflammatory bowel disease (IBD) and (ii) resistin levels may be associated with disease activity in IBD. METHODS: We addressed these questions by testing for associations between resistin plasma levels, inflammatory parameters and clinical disease activity in a case-control study with 235 patients with Crohn's disease (CD), 112 patients with ulcerative colitis (UC) and 144 healthy controls. RESULTS: Patients with IBD showed significantly higher resistin levels compared with controls (P<0.0001). In both, patients with CD and UC, resistin concentrations were significantly associated with elevated white blood cell count (P<0.0001), C-reactive protein (CRP) (P<0.0001) and disease activity (P< or =0.0001). In multivariate logistic regression analysis, resistin levels were identified as an independent predictor of active disease (odds ratio 1.014, 95% confidence interval 1.002-1.027, P=0.02) in patients with CD after adjusting for sex, age, body mass index, white blood cell count and CRP. In UC patients, resistin was associated with active disease in multivariate regression analysis after control for sex, age, body mass index and white blood cell count (odds ratio 1.015, 95% confidence interval 1.002-1.029, P=0.02). Addition of CRP, however, abolished this association. CONCLUSION: Resistin levels are an independent predictor of disease activity in patients with CD. Resistin may represent a novel link between inflammation and IBD.

Apolipoprotein A-IV is an independent predictor of disease activity in patients with inflammatory bowel disease.

BACKGROUND: ApoA-IV, an apolipoprotein (apo) with antioxidant, antiatherogenic, and antiinflammatory properties, was recently demonstrated to inhibit dextran sulfate sodium (DSS)-induced experimental colitis in mice. We therefore hypothesized that apoA-IV may be associated with disease activity in patients with inflammatory bowel disease (IBD). METHODS: We addressed this question by testing for associations between apoA-IV genotypes, apoA-IV plasma levels, inflammatory parameters, and clinical disease activity in 206 patients with Crohn's disease (CD), 95 subjects with ulcerative colitis (UC), and 157 healthy controls. RESULTS: In CD patients, apoA-IV plasma levels were inversely associated with C-reactive protein (CRP) (P = 0.005) and disease activity (P = 0.01) in univariate analysis. In multiple logistic regression analysis, apoA-IV levels were identified as an independent predictor of elevated CRP (odds ratio [OR] 0.956, 95% confidence interval [CI]: 0.916-0.998, P = 0.04) and active disease (OR 0.957, 95% CI: 0.918-0.998, P = 0.04). In UC patients the apoA-IV gene variant 360 His (P = 0.03) but not apoA-IV levels (P = 0.15) were associated with increased disease activity in univariate analysis. This association, however, was lost in multiple logistic regression analysis (OR 3.435, 95% CI 0.995-11.853, P = 0.05). CONCLUSIONS: To our knowledge, this is the first study to demonstrate an association of apoA-IV with disease activity in patients with CD. Further studies are needed to define the relationship of apoA-IV to IBD.