Changes of the cytokine profile in inflammatory bowel diseases

Abstract

Cytokines are indispensable signals of the mucosa-associated immune system for maintaining normal gut homeostasis. An imbalance of their profile in favour of inflammation initiation may lead to disease states, such as that is observed in inflammatory bowel diseases (IBD). Although Crohn's disease (CD) is often described as a prototype of T-helper 1-type diseases, and ulcerative colitis (UC) is traditionally viewed as a T-helper 2-mediated condition, the classic paradigm, which categorises cytokines into pro- and anti-inflammatory groups, has recently been changed. The inflammation regulatory pathways may not be mutually exclusive as individual cytokines can have diverse and even opposing functions in various clinical and immunological settings. None the less there are many common immunological responses in IBD that are mediated by cytokines. Although they regulate and influence the development, course and recurrence of the inflammatory process, the concrete pathogenic role of these small signaling molecules is sometimes not unambiguous in the subtypes of the disease. Our aim is to review the current information about pro- and anti-inflammatory effects of traditionally studied and recently discovered cytokines in the pathogenesis of UC and CD. The better understanding of their production and functional activity may lead to the development of new therapeutic modalities.

Keywords: Crohn’s disease; Interleukin-25; Interleukin-33; Interleukin-35; Interleukin-4; Interleukin-8; Tumor necrosis factor ligand superfamily member 14; Tumor necrosis factor-like factor; Ulcerative colitis.

Figure 1

The disease-related pathogenic role of cytokines with pro-inflammatory, anti-inflammatory and pro-fibrogenic effects in ulcerative colitis and Crohn’s disease. LIGHT: Lymphotoxins, exhibits inducible expression, and competes with herpes sipmlex virus glycoprotein D for herpesvirus entry mediator, a receptor expressed by T lymphocytes; IL: Interleukin; TNF: Tumor necrosis factor; TL1A: TNF-like factor; TGF-β: Transforming growth factor-β.