The bactericidal capacity of digestion products of bovine milk triglycerides and membrane lipids was tested in vitro using Escherichia coli O157:H7, Salmonella enteritidis, Campylobacter jejuni, Listeria monocytogenes, and Clostridium perfringens. C 10:0 and C 12:0 fatty acids and digestion products of sphingolipids appeared to be effective bactericidal agents, whereas digestion products of phosphoglycerides were moderately bactericidal. Thus, milk fat sphingolipids and triglycerides, particularly those containing C 10:0 and C 12:0 fatty acids, may protect against food-borne gastroenteritis.
During fat digestion, fatty acids and monoglycerides are liberated in the gastrointestinal tract. Generally, these lipids are potent inhibitors of gram-positive bacteria in vitro but have less effect on gram-negative microbes. Considering this, we hypothesized that increased intake of bovine milk fat would result in enhanced gastrointestinal killing of Listeria monocytogenes (gram-positive) but have little effect on infection with Salmonella enteritidis (gram-negative) in rats. To test this, rats were fed either low milk fat diets (10% of energy obtained from milk fat, corresponding to 4. 2 g fat/100 g diet) or high milk fat diets (40% of energy obtained from milk fat, corresponding to 19.6 g fat/100 g diet). After adaptation to these diets, rats were orally infected with Listeria or Salmonella. Greater milk fat consumption in Listeria-infected rats diminished intestinal colonization of Listeria (P < 0.05) and reduced diarrhea (P < 0.05). Analysis of gastrointestinal contents showed that killing of Listeria occurred predominantly in the stomach. High milk fat intake significantly augmented this gastric listericidal capacity (P < 0.05) and raised the concentration of medium-chain and saturated long-chain free fatty acids and of monoglycerides of C12:0, C14:0, C16:0, C18:0, and C18:1 in gastric chyme (P < 0.05). Considering the in vitro listericidal capacity of these agents, it was concluded that particularly the free fatty acids C10:0, C12:0 and C14:0 and the monoglycerides of C12:0, C14:0, and C16:0 seem to play a pivotal role in this enhanced Listeria killing. In contrast, Salmonella infection was not affected by milk fat consumption. In conclusion, high milk fat intake results in higher concentrations of gastric bactericidal lipids and thereby protects against Listeria infection but not against Salmonella.
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.
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