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J Dig Dis. 2013 Oct;14(10):543-51. doi: 10.1111/1751-2980.12068.

The therapeutic role of oral tolerance in dextran sulfate sodium-induced colitis via Th1-Th2 balance and γδ T cells.

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1
Department of Gastroenterology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China.

Abstract

OBJECTIVE:

To evaluate the state of oral tolerance and its therapeutic role in mice with dextran sulfate sodium (DSS)-induced colitis.

METHODS:

Delayed-type hypersensitivity (DTH) was determined 7 and 14 days after DSS-induced colitis and control mice. Disease activity index (DAI) score and colonic histopathological score were measured 7 days after colonic extracted protein (CEP) or bovine serum albumin (BSA) (control) was administrated, with the evaluation of Th1-Th2 balance in the spleen, Peyer's patch and γδ T cells in intraepithelial lymphocytes and lamina proper lymphocytes in the intestine.

RESULTS:

After fed with 250 μg ovalbumin oral tolerance was induced in 7 days in both DSS-induced colitis and control mice, while oral tolerance persisted in the control mice but vanished in DSS-induced colitis 14 days after ovalbumin challenge. DAI and colonic histopathological scores were decreased significantly after the ingestion of CEP (controlled by BSA) in DSS-induced colitis with significant reduction of Th1 and the ratio of Th1 to Th2 in Peyer's patch as well as the γδ T cells in lamina proper lymphocytes in the intestine. No significant difference in Th1-Th2 balance in the spleen and γδ T cells in intraepithelial lymphocytes in the intestine were observed.

CONCLUSIONS:

There is a defect in oral tolerance at day 7 in DSS-induced colitis. If taken orally, CEP may have a protective role in DSS-induced colitis, which may be related to the deflection from Th1 to Th2 in Peyer's patch and the reduction of γδ T cells in lamina proper lymphocytes in the intestine.

KEYWORDS:

T-lymphocytes; dextran sulfate; inflammatory bowel disease; oral tolerance; γδ T cell

PMID:
23647697
DOI:
10.1111/1751-2980.12068
[Indexed for MEDLINE]
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