Intestinal inflammatory reactions and resulting tissue injuries are two major aspects of inflammatory bowel disease (IBD). The regulatory factors involved in the pathogenesis of IBD remain unclear. Recent studies showed that musculin (MSC) as a transcription suppressor participates in the regulation of certain immune functions. The purpose of this study was to determine the impact of MSC deficiency on colonic injury and inflammatory reaction under IBD, where wild-type (WT, +/+) and MSC-knockout (MSCKO, MSC-/-) mice were induced for disease by dextran sulfate sodium (DSS) in drinking water. Immunohistochemistry hematoxylin-eosin (H&E) staining, enzyme-linked immunosorbent assay (ELISA), and quantitative real-time polymerase chain reaction (qRT-PCR) were used to analyze the matching samples from groups of different genotypes. The colonic epithelial injury in the MSC-/- IBD group was much severer than that in the +/+ IBD group, concurrent with higher IL-22 levels from the supernatant of ex vivo cultured colon tissues in the MSC-/- IBD group than those in the +/+ IBD group. The mRNA levels of IL-22 in mesenteric lymph nodes (MLN) also manifested similar tendency. MSC deficiency may enhance the inflammatory reactions in the gut via excessive secretion of IL-22, leading to aggravated colonic epithelial injury under IBD.
Keywords: colonic injury; inflammation; inflammatory bowel disease (IBD); musculin (MSC).