Intestinal
fibrosis is a common outcome of
inflammatory bowel diseases (IBDs), becoming clinically apparent in 40% of patients with
Crohn's disease and 5% of those with
ulcerative colitis. Effective pharmacological treatments aimed at controlling or reversing
fibrosis progression are unavailable.
Fibrosis is characterized by an excessive local accumulation of
extracellular matrix proteins (mainly
collagen), as a result of their increased production by activated myofibroblasts and/or their reduced degradation by specific
matrix metalloproteinases. Initiation and progression of
fibrosis are modulated by several pro- and anti-fibrogenic molecules. In recent years, the
cytokine interleukin-17 (IL-17) has been integrated into the pathogenesis of
fibrosis, although its precise contribution to IBD, and especially to its related intestinal
fibrosis, remains controversial. Several data suggest both a pro-inflammatory and pro-fibrotic action and a protective function of the Th17/IL-17 immune response. A recent study has demonstrated that the treatment with anti-IL-17 antibody significantly alleviated
2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colorectal
fibrosis in mice by down-regulating the expression of
collagen 3 and several pro-fibrogenic
cytokines. Here, we describe and discuss the possible involvement of the Th17/IL-17 immune response in the initiation ad progression of intestinal
fibrosis.