Interleukins IL-33 and IL-17/IL-17A in patients with ulcerative colitis.
ABSTRACT Disturbance of immune homeostasis in ulcerative colitis (UC) is related to the predominance of T-helper-2 (Th2) immune response. Interleukin (IL)-33 stimulates Th lymphocytes to produce Th2 cytokines, such as IL-4, IL-5, and IL-13, which are believed to induce pathological changes in the intestinal mucosa. The pro-inflammatory role of IL-17 in UC is still unclear. Our aim was to determine serum concentrations of IL-33 and IL-17 in patients with UC and healthy controls.
Serum concentrations of IL-33 and IL-17 were measured in 18 patients (10 men) with UC and 16 control subjects (10 men) by using two-layer immunoenzyme procedure (ELISA).
Median serum concentrations of IL-33 in patients with UC and controls were 140 pg/ mL (interquartile range [IQR], 72.5 pg/mL) and 165 pg/mL (IQR, 140.0 pg/mL), respectively, but the difference was not statistically significant (Mann-Whitney U=112, p = 0.281). The median serum concentration of IL-17/IL-17A in patients with UC was significantly higher (100 pg/mL, IQR 35.75pg/mL) than that in controls (65 pg/ mL, IQR 32.25 pg/mL) (Mann-Whitney U=55, p = 0.002).
Serum concentration of IL-33 in patients with UC was not increased in comparison with that in controls, which is in accordance with current evidence that its primary biological effect is transcriptional rather than cytokinal. Further research is needed to explain whether increased concentration of IL-17 in UC is protective or harmful and to elucidate its immunological and pathogenic role.
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ABSTRACT: Interleukin (IL)-33 is a new member of the IL-1 superfamily of cytokines that is expressed by mainly stromal cells, such as epithelial and endothelial cells, and its expression is upregulated following pro-inflammatory stimulation. IL-33 can function both as a traditional cytokine and as a nuclear factor regulating gene transcription. It is thought to function as an 'alarmin' released following cell necrosis to alerting the immune system to tissue damage or stress. It mediates its biological effects via interaction with the receptors ST2 (IL-1RL1) and IL-1 receptor accessory protein (IL-1RAcP), both of which are widely expressed, particularly by innate immune cells and T helper 2 (Th2) cells. IL-33 strongly induces Th2 cytokine production from these cells and can promote the pathogenesis of Th2-related disease such as asthma, atopic dermatitis and anaphylaxis. However, IL-33 has shown various protective effects in cardiovascular diseases such as atherosclerosis, obesity, type 2 diabetes and cardiac remodeling. Thus, the effects of IL-33 are either pro- or anti-inflammatory depending on the disease and the model. In this review the role of IL-33 in the inflammation of several disease pathologies will be discussed, with particular emphasis on recent advances.Journal of Inflammation 08/2011; 8(1):22. · 2.55 Impact Factor