Sweet buttermilk intake reduces colonisation and translocation ofListeria monocytogenesin rats by inhibiting mucosal pathogen adherence

Abstract

The bovine milk fat globule membrane (MFGM) contains several antimicrobial components with proven efficacyin vitro, butin vivoevidence is scarce. The present study was performed to determine the efficacy of the bovine MFGMin vivo.Rats were fed diets based on bovine skimmed milk powder (low in MFGM) or bovine sweet buttermilk powder (high in MFGM). After dietary adaptation, rats were orally infected withSalmonella enteritidisorListeria monocytogenes.Whereas sweet buttermilk powder did not protect rats against infection withS. enteritidis, it protected againstL. monocytogenes, as shown by a lower colonisation and translocation of this pathogen. Protection coincided with higher listericidal capacity of gastric and caecal contents. The digestion products of phosphoglycerides and sphingomyelin are bactericidalin vitro.To study their role, rats were fed diets containing either 0·1 % phosphatidylcholine or sphingomyelin, or a control diet. After dietary adaptation, rats were infected withL. monocytogenes.SinceListeriacolonisation was not affected by these diets, phosphoglycerides and sphingomyelin are not involved in the protective effect of sweet buttermilk. Additionalin vitroexperiments were performed to further explore the mechanism of the beneficial effects of sweet buttermilk. Inhibition of the adherence ofL. monocytogenesto the intestinal mucosa is the most likely explanation, since sweet buttermilk powder inhibited the binding ofL. monocytogenesin both a haemagglutination assay and a Caco-2 cell adherence assay. In conclusion, sweet buttermilk powder, which is rich in MFGM, protects againstL. monocytogenesinfection in rats, probably by preventing adherence of this pathogen to the intestinal mucosa.