Bifidobacterium animalis protects intestine from damage induced by zinc deficiency in rats

We investigated the potential beneficial effects of Bifidobacterium animali s on intestinal damage using zinc-deficient (ZD) rats as a model for intest inal alterations. The ZD rats were fed diets containing 1 mg Zn/kg for 20 ( ZD(20)) or 40 (ZD(40)) d to induce damage that differed in severity. Subgro ups of these rats, the ZD(20) + B and ZD(40) + B groups, received a suspens ion of B. animalis (3.5 x 10(8) colony forming units) daily for the last 10 d. Another subgroup, the ZD(40) + B + 7 d group, was fed the ZD diet for 7 d after the B. animalis treatment period. Zinc deficiency induced ulcerati ons, edema, inflammatory cell infiltration and dilatation of blood vessels in duodenum, jejunum and ileum, with increasing severity between 20 and 40 d of zinc deficiency. The mucosa of the ZD(40) + B group was well preserved , and most of the morphologic alterations induced by zinc deficiency were n ormalized in the ZD(40) + B group. The high fecal concentrations of B. anim alis in the ZD(40) + B and ZD(40) + B + 7 d groups indicate that these bifi dobacteria survived passage through the gastrointestinal tract and prolifer ated. Electron microscopy confirmed the elevated numbers of bifidobacteria in cecum. Treatment with B. animalis resulted in greater epithelial cell pr oliferation and disaccharidase activities in the ZD(40) + B group compared with the ZD(40) group. These findings indicate that B. animalis can protect the intestine from alterations induced by zinc deficiency, suggesting that this bacterium may play a role in intestinal mucosal defense.