In order to know the effect of pre-existing Trichinella spiralis infection on experimentally induced intestinal inflammation and immune responses, we induced colitis in T. spiralis-infected mice and observed the severity of colitis and the levels of Th1, Th2, and regulatory cytokines and recruitment of CD4+CD25+Foxp3+ T (regulatory T; Treg) cells. Female C57BL/6 mice were infected with 250 muscle larvae; after 4 weeks, induction of experimental colitis was performed using 3% dextran sulfate sodium (DSS). During the induction period, we observed severity of colitis, including weight loss and status of stool, and evaluated the disease activity index (DAI). A significantly low DAI and degree of weight loss were observed in infected mice, compared with uninfected mice. In addition, colon length in infected mice was not contracted, compared with uninfected mice. We also observed a significant increase in production of pro-inflammatory cytokines, IL-6 and IFN-gamma, in spleen lymphocytes treated with DSS; however, such an increase was not observed in infected mice treated with DSS. Of particular interest, production of regulatory cytokines, IL-10 and transforming growth factor (TGF)-beta, in spleen lymphocytes showed a significant increase in mice infected with T. spiralis. A similar result was observed in mesenteric lymph nodes (MLN). Subsets of the population of Treg cells in MLN and spleen showed significant increases in mice infected with T. spiralis. In conclusion, T. spiralis infection can inhibit the DSS-induced colitis in mice by enhancing the regulatory cytokine and Treg cells recruitment.
Animals ; Colitis/chemically induced/*immunology/pathology ; Cytokines/genetics/*immunology/metabolism ; Dextran Sulfate/adverse effects ; Disease Models, Animal ; Female ; Forkhead Transcription Factors/immunology/metabolism ; *Gene Expression Regulation ; Larva ; Mice ; Mice, Inbred C57BL ; Spleen/immunology ; T-Lymphocytes, Regulatory/*immunology ; Trichinella spiralis/*immunology ; Trichinellosis/*immunology/parasitology

The involvement of mucosal mast cells (MMC) in the pathophysiology of irritable bowel syndrome (IBS) is still controversial. We aimed to re-evaluate the role of MMC in visceral hypersensitivity associated with IBS using a rat IBS model that develops the IBS symptom after a subsidence of acetic acid-induced colitis. No significant difference in the number of MMC was observed between normal rat colon and IBS rat colon. (61.7 +/-2.9/mm 2 in normal vs. 88.7 +/-13.3/mm 2 in IBS, p >0.29). However, the degranulation rate of MMC was significantly higher in IBS rat colon (49.5 +/-2.4% in normal vs. 68.8 +/-3.4% in IBS, p >0.05). Pretreatment of a mast cell stabilizer, doxantrazole (5 mg/kg, i.p.), reduced the degranulation rate of MMC and significantly attenuated visceral hypersensitivity to rectal distension in IBS rat, whereas it had no effect on the visceral sensory responses in normal rat. These results suggest that, although the number of MMC is not significantly changed in IBS rat colon, the higher degranulation rate of MMC is responsible for visceral hypersensitivity in this model IBS.
Acetic Acid/toxicity ; Animals ; Cell Count ; Colitis/chemically induced/*pathology ; Hypersensitivity/*pathology ; Image Processing, Computer-Assisted ; Intestinal Mucosa/*pathology ; Irritable Bowel Syndrome/*pathology ; Male ; Mast Cells/drug effects/*pathology ; Models, Theoretical ; Phosphodiesterase Inhibitors/pharmacology ; Rats ; Rats, Sprague-Dawley ; Thioxanthenes/pharmacology ; Viscera/immunology ; Xanthones/pharmacology