title: Dietary calcium inhibits the intestinal colonization and translocation of Salmonella in rats.
abstract: OBJECTIVE
  Dietary calcium decreases the cytotoxicity of intestinal contents and intestinal epitheliolysis by precipitating cytotoxic surfactants such as bile acids. A decreased luminal cytotoxicity might not only strengthen the barrier function of the gut mucosa but also reinforce the protective, endogenous microflora. We hypothesized, therefore, that dietary calcium increases the resistance to intestinal infections.
  
  
  METHODS
  Rats on a low-, medium-, or high-calcium purified diet were orally infected with a single dose of Salmonella enteritidis. The kinetics of fecal Salmonella excretion was studied to determine the colonization resistance. Intestinal bacterial translocation was quantitated by measuring urinary oxidation products of nitric oxide (NOx) excretion and culturing bacteria from tissues.
  
  
  RESULTS
  Compared with the low-calcium group, the medium- and high-calcium diet-fed rats had a substantially improved colonization resistance. Calcium supplementation also reduced translocation of Salmonella, considering the diminished urinary NOx excretion and viable Salmonella counts in the Ileal Peyer's patches and spleen. Dietary calcium decreased the bile acid concentration and cytotoxicity of fecal water. Several indicators of fecal bacterial mass were significantly increased by supplemental calcium.
  
  
  CONCLUSIONS
  Dietary calcium improves the colonization resistance and reduces the severity of gut-derived systemic infections, which is probably attributable to its luminal cytoprotective effects.
authors.affiliation: Department of Nutrition, Netherlands Institute for Dairy Research, Ede, The Netherlands.
authors.forename: I M
authors.initials: IM
authors.lastname: Bovee-Oudenhoven
authors.forename: D S
authors.initials: DS
authors.lastname: Termont
authors.forename: A H
authors.initials: AH
authors.lastname: Weerkamp
authors.forename: M A
authors.initials: MA
authors.lastname: Faassen-Peters
authors.forename: R
authors.initials: R
authors.lastname: Van der Meer
mesh_terms: D000818:Animals; D018988:Bacterial Translocation / Q000187:drug effects* / Q000502:physiology; D001647:Bile Acids and Salts / Q000032:analysis / Q000378:metabolism; D002136:Calcium, Dietary / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004435:Eating / Q000502:physiology; D005243:Feces / Q000737:chemistry / Q000382:microbiology; D007410:Intestinal Diseases / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000382:microbiology*; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D008903:Minerals / Q000032:analysis / Q000378:metabolism; D009566:Nitrates / Q000652:urine; D009573:Nitrites / Q000652:urine; D009584:Nitrogen / Q000032:analysis / Q000378:metabolism; D010581:Peyer's Patches / Q000382:microbiology; D010758:Phosphorus / Q000032:analysis / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012481:Salmonella Infections, Animal / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D012477:Salmonella enteritidis / Q000302:isolation & purification / Q000502:physiology*; D013154:Spleen / Q000382:microbiology; D014867:Water / Q000032:analysis
chemical_list: D001647:Bile Acids and Salts; D002136:Calcium, Dietary; D008903:Minerals; D009566:Nitrates; D009573:Nitrites; D014867:Water; D010758:Phosphorus; D009584:Nitrogen