Abstract
Interleukin 17A (IL-17A) and interleukin 17F (IL-17F) appear to play important role in pathogenesis of some autoimmune diseases. However, their role in inflammatory bowel disease (IBD) has not been yet fully elucidated. We aimed to determine serum IL-17A and IL-17F in children with IBD and to assess their association with IBD activity. Recruited children underwent blood tests including complete blood count, C-reactive protein, erythrocyte sedimentation rate, IL-17A and IL-17F and stool sampling for calprotectin. The study group comprised 68 children with IBD, including 43 with ulcerative colitis and 25 with Crohn’s disease. Control group included 20 healthy children. IL-17A was significantly increased in children with IBD (median: 10.95 pg/ml; range: 0.65–200.54 pg/ml) compared to controls (median: 4.09 pg/ml; range: 0.67–26.20 pg/ml) (p = 0.002). IL-17A was significantly increased in patients with active phase of ulcerative colitis (median: 14.58 pg/ml; range: 0.65–200.54 pg/ml) compared to those in ulcerative colitis remission (median: 8.13 pg/ml; range: 1.61–58.56 pg/ml) (p = 0.04). There were no significant differences in IL-17A among patients with active and inactive Crohn’s disease (p = 0.18). IL-17F did not differ significantly between children with IBD (median: 15.11 pg/ml; range: 0.09–189.84 pg/ml) and controls (median: 11.56 pg/ml; range: 0.19–32.49 pg/ml) (p = 0.33). Our study suggests that interleukin 17A may diverse active phase from remission only in ulcerative colitis but not in Crohn’s disease.
Highlights
Inflammatory bowel disease (IBD) is a group of chronic disorders of gastrointestinal tract with multifactorial and complex pathogenesis which has not been fully e lucidated[1]
We found that serum Interleukin 17A (IL-17A) was significantly increased in patients with active phase of ulcerative colitis compared to those in ulcerative colitis remission (p = 0.04)
One of cytokines which has been recently explored in terms of inflammatory bowel disease (IBD) pathogenesis is IL-17A
Summary
Inflammatory bowel disease (IBD) is a group of chronic disorders of gastrointestinal tract with multifactorial and complex pathogenesis which has not been fully e lucidated[1]. IBD-unclassified is a form of IBD colitis with features that make uncertain the differentiation between ulcerative colitis and Crohn’s disease at diagnosis[2] These diseases constitute distinct entities, it is hypothesised that IBD in general may occur in genetically susceptible individuals as a result of impaired immune response and alteration of gut microbiota triggered by environmental factors[1]. Disruption of both innate and adaptive immune responses are considered to play role in the pathogenesis of I BD3–5.
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