Bovee-Oudenhoven I M, Wissink M L, Wouters J T, Van der Meer R
Section Nutrition & Health, NIZO Food Research, 6710 BA Ede, The Netherlands.
J Nutr. 1999 Mar;129(3):607-12. doi: 10.1093/jn/129.3.607.
We have shown recently that dietary calcium phosphate (CaPi) has a trophic effect on the intestinal microflora and strongly protects against salmonella infection. It was speculated that precipitation by CaPi of intestinal surfactants, such as bile acids and fatty acids, reduced the cytotoxicity of intestinal contents and favored growth of the microflora. Because lactobacilli may have antagonistic activity against pathogens, the main purpose of the present study was to examine whether this CaPi-induced protection coincides with a reinforcement of the endogenous lactobacilli. In vitro, Salmonella enteritidis appeared to be insensitive to bile acids and fatty acids, whereas Lactobacillus acidophilus was killed by physiologically relevant concentrations of these surfactants. Additionally, after adaptation to a purified diet differing only in CaPi concentration (20 and 180 mmol CaHPO4. 2H2O/kg), rats (n = 8) were orally infected with S. enteritidis. Besides reducing the cytotoxicity and the concentration of bile acids and fatty acids of ileal contents and fecal water, CaPi notably changed the composition of ileal bile acids in a less cell-damaging direction. Significantly greater numbers of ileal and fecal lactobacilli were detected in noninfected, CaPi-supplemented rats. As judged by the lower urinary NOx excretion, which is a biomarker of intestinal bacterial translocation, dietary CaPi reduced the invasion of salmonella. Additionally, the colonization resistance was improved considering the reduction of excreted fecal salmonella. In accordance, fewer viable salmonella were detected in ileal contents and on the ileal mucosa in the CaPi group. In conclusion, reducing the intestinal surfactant concentration by dietary CaPi strengthens the endogenous lactobacilli and increases the resistance to salmonella.
我们最近发现,膳食磷酸钙(CaPi)对肠道微生物群具有营养作用,并能有效预防沙门氏菌感染。据推测,CaPi使肠道表面活性剂(如胆汁酸和脂肪酸)沉淀,降低了肠内容物的细胞毒性,有利于微生物群的生长。由于乳酸杆菌可能对病原体具有拮抗活性,本研究的主要目的是检验这种由CaPi诱导的保护作用是否与内源性乳酸杆菌的增强相吻合。在体外,肠炎沙门氏菌似乎对胆汁酸和脂肪酸不敏感,而嗜酸乳杆菌会被这些表面活性剂的生理相关浓度杀死。此外,在适应仅CaPi浓度不同(20和180 mmol CaHPO4·2H2O/kg)的纯化饮食后,大鼠(n = 8)经口感染肠炎沙门氏菌。除了降低回肠内容物和粪便水的细胞毒性以及胆汁酸和脂肪酸的浓度外,CaPi还显著改变了回肠胆汁酸的组成,使其朝着对细胞损伤较小的方向变化。在未感染且补充CaPi的大鼠中,检测到回肠和粪便中的乳酸杆菌数量显著增多。根据较低的尿NOx排泄量(肠道细菌易位的生物标志物)判断,膳食CaPi减少了沙门氏菌的侵袭。此外,考虑到粪便中排出的沙门氏菌减少,定植抗力得到改善。相应地,在CaPi组的回肠内容物和回肠黏膜上检测到的活沙门氏菌较少。总之,通过膳食CaPi降低肠道表面活性剂浓度可增强内源性乳酸杆菌,并增加对沙门氏菌的抵抗力。