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Lactococcus lactis attenuates murine colitis by lowering oxidative stress
▸ Ballal SA, Veiga P, Fenn K, et al. Host lysozyme-mediated lysis of Lactococcus lactis facilitates delivery of colitis-attenuating superoxide dismutase to inflamed colons. Proc Natl Acad Sci 2015;112:7803–8.
Oxidative stress contributes to chronic inflammation and dysbiosis in IBD. Finding ways to lessen oxidative stress may help to restore homeostasis in the intestine. Identifying microbes that target pathways such as oxidative stress provide stepping-stones towards new IBD therapies. Earlier work by Garrett's laboratory established that fermented milk containing five bacterial strains could be used to reduce colitis in an innate immune model of colitis. In the present study, Ballal and colleagues sought to determine the contributions of each of these strains to attenuating colitis. The group found that one strain, L. lactis l-1631, reduced gut oxidative stress and attenuated colitis in three mouse models of colonic inflammation: BALB/c T-bet−/− Rag2−/− mice, BALB/c Il10−/− mice and BALB/c wild-type mice treated with DSS. L. lactis I-1631, a bacterium used in the dairy industry, has not been widely recognised as a beneficial microbe. Interestingly, the beneficial effect of L. lactis was not mediated by anti-inflammatory properties but was rather dependent on endogenous production of SodA, which reduced colonic epithelial reactive oxygen species. SodA is located in the cytoplasm of L. lactis and not secreted, so how can it mediate an effect in the host's intestine? The authors’ data indicate that lysozyme-mediated lysis at inflamed colonic areas contributes to L. lactis's release of its cytoplasmic SodA, which is necessary for L. lactis's colitis-attenuating activity. Lysozyme expression is substantially increased in the inflamed colon of mice and humans. Should L. lactis be used in therapy? This natural targeting mechanism will ensure that the bacteria exert its effect only where it is needed. Of special note, L. lactis is generally regarded …