Objective: To study the expressions of interleukin-17 (IL-17) and interleukin-23 (IL-23) in the intestinal mucosa of BABL/C mice infected with Blastocystis hominis.
Methods: A total of 30 BABL/C mice were randomly divided into different groups: an experimental group, an immunosuppressant group and a normal group. Each mouse of the experimental group and immunosuppressant group was administered intraperieneally with dexamethasone (2 mg, gd, for 5 days) and one of the control group was given physiological saline (0.2 ml). In the experimental group, each mouse was infected with Blastocystis hominis (107 parasites per 0.5 ml) by the intragastric infusion method; in the immunosuppressant group and normal group, the mice were fed with equal physiological saline. On the fifth day post-infection, the duodenum, jejunum, ileum and colon of the mice of the 3 groups were taken out for the tissue section. The pathological changes of bowel mucosa were determined by HE staining, and the expressions of IL-17 and IL-23 in different parts of bowel mucosa were determined by immunohistochemistry assay.
Results: The pathological examinations showed intestinal mucosa had various degrees of inflammatory changes. The expressions of IL-17 and IL-23 in the intestinal mucosa of the mice in the experimental group was significantly higher than those in the immunosuppressant group or normal group (both P < 0.05). The expressions of IL-17 and IL-23 in the intestinal mucosa of the mice in the immunosuppressant group were similar to those in the normal group (P > 0.05). The expression of IL-17 in the duodenum or jejunum or colon of the mice was significantly higher than that in the ileum in the experimental group (P < 0.05). The expression of IL-23 in the duodenum or jejunum of the mice was significantly higher that that in the ileum or colon in the experimental group (P < 0.05).
Conclusions: IL-17 and IL-23 are highly expressed in the intestinal mucosa of the mice infected with Blastocystis hominis. IL-23 may also be involved in the immunomodulatory effects of Blastocystis hominis infection, which plays a mutual regulatory role with IL-17.