Literature DB >> 17075345

Improvement of an experimental colitis in rats by lactic acid bacteria producing superoxide dismutase.

Wei Han1, Annick Mercenier, Afifa Ait-Belgnaoui, Sonia Pavan, Florence Lamine, Iris I van Swam, Michiel Kleerebezem, Christel Salvador-Cartier, Michael Hisbergues, Lionel Bueno, Vassilia Theodorou, Jean Fioramonti.   

Abstract

The use of superoxide dismutases (SODs) in inflammatory diseases is hampered by their short circulatory half-life. To determine whether a bacterial supply of SOD into the colon might improve an experimental colitis, the effects of oral treatment with live recombinant lactic acid bacteria producing different amounts of SOD and those of colonic infusion of SOD were compared. Wistar rats were fitted with a catheter in the proximal colon through which TNBS was administered to induce colitis. Animals received a continuous intracolonic infusion of bovine SOD (40 U per rat per day) for 4 days after TNBS or were treated orally with live recombinant Lactococcus lactis or Lactobacillus plantarum strains (10 colony-forming units (CFU)/d), producing or not producing SOD, for 4 days before and after TNBS. SOD activity of bacterial extracts was 0, 26, 74, and 624 units/10 CFU for L. plantarum, L. lactis, L. lactis SOD, and L. plantarum SOD, respectively. Four days after TNBS, macroscopic and microscopic damage, myeloperoxidase (MPO) activity, and nitrotyrosine immunostaining were evaluated. TNBS induced macroscopic and microscopic damages, an increase in MPO activity, and intense immunostaining for nitrotyrosine. Macroscopic damage and MPO activity were reduced by bovine SOD. These parameters and microscopic damages also were reduced by L. lactis, L. lactis SOD, and L. plantarum SOD, but not by L. plantarum. Nitrotyrosine immunostaining was attenuated after treatment with the 4 bacterial strains. Although not all of the anti-inflammatory effects could be attributed directly to SOD, our results suggest that SOD-producing lactic acid bacteria open a novel approach in inflammatory bowel disease treatment.

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Year:  2006        PMID: 17075345     DOI: 10.1097/01.mib.0000235101.09231.9e

Source DB:  PubMed          Journal:  Inflamm Bowel Dis        ISSN: 1078-0998            Impact factor:   5.325


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