Interleukin-18 upregulation is associated with the use of steroids in patients with ulcerative colitis

This is the authors' abstract. We don't add key points for this paper.

To the Editor: Inflammatory bowel disease (IBD) comprises two forms, ulcerative colitis (UC) and Crohn's disease (CD). Currently, the pathogenesis of IBD is not completely understood. Cytokines are key signals in the intestinal immune system and are known to participate in the disruption of the so-called normal state of controlled inflammation (physiological inflammation of the gut).1 In both diseases an increased production of interleukin (IL-1), IL-6, tumor necrosis factor alpha (TNF-α), and IL-18 have been reported in the inflamed mucosa.2 Interleukin-18 is a cytokine that initiates and promotes host defense and inflammation.3 IL-18 is related by mechanism of origin, receptor structure, and signal pathway with IL-33 and IL-1.3,4 The activation of the NLRP3 inflammasome results in IL-1 and IL-18 production for the conversion of pro-caspase-1 to caspase 1 followed by the cleavage of pro-interleukins 1 and 18. Another source of IL-18 production is represented by macrophages, keratinocytes, Kupffer cells, and intestinal epithelial cells that produce and secrete IL-18.2,4,5