Interleukins IL-33 and IL-17/IL-17A in Patients with Ulcerative Colitis

Hepato-gastroenterology (Impact Factor: 0.93). 11/2009; 57(104):1442-4.
Source: PubMed


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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    • "In this regard, Beltrán et al. found increased IL-33 levels in the serum of patients with IBD, but no correlation with disease activity was observed [18]. In contrast, Ajduković et al. found no difference in IL-33 serum levels between 18 individuals with UC and healthy controls, suggesting that the role of IL-33 in UC might be posttranscriptional since they could not find any increase in cytokine levels in affected subjects [22]. Later, however, Pastorelli et al. clearly demonstrated that IL-33 serum levels were indeed higher in UC and CD patients compared with controls with no difference between both types of IBD [16]. "
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    ABSTRACT: Interleukin- (IL-) 33 is a widely expressed cytokine present in different cell types, such as epithelial, mesenchymal, and inflammatory cells, supporting a predominant role in innate immunity. IL-33 can function as a proinflammatory cytokine inducing Th2 type of immune response being involved with the defense against parasitic infections of the gastrointestinal tract. In addition, it has been proposed that IL-33 can act as a signaling molecule alerting the immune system of danger or tissue damage. Recently, in the intestinal mucosa, overexpression of IL-33 has been reported in samples from patients with inflammatory bowel diseases (IBD). This review highlights the available data regarding IL-33 in human IBD and discusses emerging roles for IL-33 as a key modulator of intestinal inflammation.
    Full-text · Article · Feb 2014 · Mediators of Inflammation
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    • "Serum IL-33 and sST2 levels were elevated in UC patients compared with controls, while anti-TNF treatment decreased circulating IL-33 and increased sST2, thus favorably altering the ratio of the cytokine with its decoy receptor [74]. However, in other studies serum concentrations of IL-33 were low or did not differ between UC patients and healthy controls [75,78]. "
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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.
    Full-text · Article · Aug 2011 · Journal of Inflammation
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    ABSTRACT: The mechanisms underlying the chronic intestinal inflammation that is a hallmark of inflammatory bowel diseases (IBD) are complex. Components of the pathological response include the adaptive and innate immune systems, as well as the intestinal epithelium and endothelium. Advances in the understanding of the roles of each of these components have resulted in the development of multiple biological agents that all represent an alternative to the use of current therapies in patients with refractory Crohn's disease or ulcerative colitis. This study systematically reviews the mechanisms of action, efficacy and safety of new and emerging therapies that are currently in clinical trials and discusses future directions in the treatment of IBD.
    No preview · Article · Nov 2011 · Gut
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