[IL-16 aggravates dextran sulfate sodium (DSS)-induced mouse inflammatory bowel disease by promoting M1 polarization...

Objective To investigate the role of interleukin-16 (IL-16) in the development of inflammatory bowel disease (IBD) and clarify its regulatory mechanism involved in the pathogenesis of IBD. Methods Seven-week-old wild-type C57BL/6 (WT) and IL-16 knockout (IL-16^-/-) female mice were divided into WT control group, WT dextran sulfate sodium (DSS) treatment group, IL-16^-/- control group and IL-16^-/- DSS treatment group. The DSS model groups were given the water with 25 g/L DSS for 7 days to establish the IBD models, while the control groups were given the normal water. During the modeling period, the body mass of mice was recorded to calculate the body mass curve. After 7 days, the whole colon of the mice was dissected and the level of IL-16 mRNA in the colon tissue was detected by real-time PCR. The level of IL-16 protein in the colon tissue was detected by ELISA. The expression and localization of IL-16 in the colon tissue were observed by immunofluorescence technique. HE staining was used to detect colonic pathological injury in mice. TUNEL assay was used to detect cell apoptosis of the colon tissue. Flow cytometry was used to detect the number and polarization of macrophages in peritoneal cells (F4/80, CD86). Immunohistochemical staining was used to detect the distribution of macrophages in the colon tissues. Real-time PCR was used to detect IL-6 and IL-12 mRNA levels in the colon tissue, and IL-6 and IL-12 protein levels were detected by ELISA. Results DSS induced high expression of IL-16 in the colon tissue. Compared with WT DSS treatment group, IL-16^-/- DSS treatment group showed less changes in body mass, less colon tissue damage, and markedly lower percents of apoptotic cells in the peritoneal or colonic tissues of IL-16^-/- mice. What's more, the number of macrophages, the polarization level of M1 macrophages, and the levels of the iconic inflammatory factors IL-6 and IL-12 significantly decreased in IL-16^-/- DSS treatment group compared with WT DSS treatment group. Conclusion IL-16 can aggravate DSS-induced IBD by promoting the polarization of M1 macrophages.