Effects of a Lactobacillus reuteri BR11 Mutant Deficient in the Cystine-Transport System in a Rat Model of Inflammatory Bowel Disease
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Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract associated with altered composition of the gut microbiota. Lactobacillus reuteri BR11 (BR11) has recently been reported to reduce the severity of experimental IBD because of its probiotic properties possibly attributed to a mechanism of thiol production via its unique cysteine/cystine-transport system.
We compared BR11 and a BR11 mutant deficient in the cystine-uptake system (PNG201), for their capacity to reduce the severity of experimental colitis.
Male Sprague–Dawley rats (n = 8 per group) were gavaged (1 ml/day) with skim milk, BR11 or PNG201 (1 × 109 CFU/ml) for 12 days. Rats consumed either water or 2% dextran sulfate sodium in drinking water from days 6 to 12 to induce colitis. Metabolism data, disease activity index, intestinal mucin profile, and histological analyses were assessed and compared by ANOVA.
Assessed histologically, DSS administration resulted in significant colonic deterioration, including loss of crypt area and increased damage severity. BR11 administration only partially alleviated the DSS effects, with a minor improvement in crypt area (P < 0.05). Administration of the PNG201 mutant strain to colitic animals failed to achieve significance (P > 0.05) against the DSS control for any of the end-points. However, the mutant strain induced significantly greater (P < 0.05) histological severity compared with BR11-treated colitic animals, indicative of possible exacerbation of colitis.
The cystine-uptake system only minimally affects the biological effects of BR11, as evidenced by histological and macroscopic colitic changes.
KeywordsColon Dextran sulfate sodium Inflammatory bowel disease Lactobacillus reuteri Probiotic Ulcerative colitis
Dr Ashis Samanta and Kerry Lymn assisted in conducting the animal trials. Dr Roger Yazbek assisted in interpretation of results. This work was funded in-part by a grant from the Cancer Council South Australia and by the National Health and Medical Research Council of Australia. Professor Gordon Howarth is supported by the Sally Birch Cancer Council Australia Senior Research Fellowship in Cancer Control.
Conflict of interest
None of the authors has any conflict of interest.
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