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LETTERS TO THE EDITOR
Neurogastroenterology and Nutrition Unit, National Institute for Agricultural Research, Toulouse, France
TO THE EDITOR: We have read with interest the recent paper by Carroll et al. (1) showing that a treatment with Lactobacillus gasseri engineered to produce superoxide dismutase (SOD) reduces the spontaneous colitis observed in interleukin 10 (IL-10)-deficient mice. Four months before the authors submitted their paper for publication, we published very similar results, and we regret that the authors failed to refer to our published work. The only differences were that instead of L. gasseri, we used L. plantarum and Lactococcus lactis also engineered to express SOD, and instead of IL-10 deficient mice, we induced a colitis with trinitrobenzene sulfonic acid (TNBS) in rats.
Nevertheless, it is very interesting to have a finding confirmed in other experimental conditions. The animal model of colitis is important to assess the anti-inflammatory properties of a probiotic. For example, an absence of effect of L. plantarum 299V has been reported against a TNBS-induced colitis (3), whereas the same strain reduced the colitis of IL-10-deficient mice (5). In the paper by Carroll et al. (1) and ours, common parameters of inflammation (histological score, neutrophil infiltration) were analyzed, and in both papers some effects of the wild-type bacteria have been observed, indicating that all the anti-inflammatory properties did not depend on SOD overexpression. This is clearly emphasized in a recent paper (4) in which L. casei producing a catalase had the same anti-inflammatory effect against a DSS-induced colitis in mice than the wild-type, which does not express catalase. There are evidently similarities in the discussion of the two papers (10 cited references are common), but there is an interesting divergence in the hypotheses of mechanisms of action. Carroll et al. believe that the bacteria must survive in the gastrointestinal tract to be active, and they measure this survival. On the contrary, we believe that a lysis is necessary to render SOD available in the colonic content.
In conclusion, the role of reactive oxygen metabolites (ROMs) is well established in inflammatory bowel diseases and the use of enzymes that neutralize ROMs has been considered as a promising way of treatment, but therapeutic uses of SOD are hampered by its short circulatory half-life of only 5–10 min. The two papers clearly demonstrate that the local colonic delivery of SOD by bacteria is effective to reduce an experimental colitis. The use of genetically modified bacteria in humans remains difficult to date, but the use of wild-type bacteria selected for their production of SOD, and/or other enzymes neutralizing ROMs, may be a promising means of inflammatory bowel disease treatment.
Address for reprint requests and other correspondence: J. Fioramonti, Neurogastroenterology and Nutrition Unit, INRA, 180 chemin de Tournefeuille, BP 3, 31931 Toulouse cedex 9, France (e-mail: jfioramo{at}toulouse.inra.fr)
REFERENCES
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