Bovee-Oudenhoven I M, Termont D S, Heidt P J, Van der Meer R
Department of Nutrition, Netherlands Institute for Dairy Research, Ede, The Netherlands.
Gut. 1997 Apr;40(4):497-504. doi: 10.1136/gut.40.4.497.
Lactulose fermentation by the intestinal microflora acidifies the gut contents, resulting in an increased resistance to colonisation by acid sensitive pathogens. The extent of fermentation should be controlled to prevent acid induced epithelial cell damage. Considering the buffering capacity of calcium phosphate and its intestinal cytoprotective effects, whether supplemental calcium phosphate adds to the increased resistance to intestinal infections by lactulose fermentations was studied.
In a strictly controlled experiment, rats were fed a purified low calcium control diet, a low calcium/lactulose diet, or a high calcium/lactulose diet, and subsequently infected orally with Salmonella enteritidis.
Lactulose fermentation lowered the pH and increased the lactic acid concentration of the intestinal contents, which significantly reduced excretion of this pathogen in faeces; thus it improved the resistance to colonisation. This agreed with the high sensitivity of S enteritidis to lactic acid (main metabolite of lactulose fermentation) in vitro. Calcium phosphate decreased translocation of S enteritidis to the systemic circulation, an effect independent of lactulose. The unfavourable increased cytotoxicity of faecal water caused by lactulose fermentation was more than counteracted by supplemental calcium phosphate. Moreover, calcium phosphate stimulated lactulose fermentation, as judged by the reduced lactulose excretion in faeces and increased lactic acid, ammonia, and faecal nitrogen excretion.
Extra calcium phosphate added to a lactulose diet improves the resistance to colonisation and translocation of S enteritidis. This is probably mediated by a calcium induced stimulation of lactulose fermentation by the intestinal microflora and reversion of the lactulose mediated increased luminal cytotoxicity, which reduces damage inflicted on the intestinal mucosa.
肠道微生物群对乳果糖的发酵可使肠道内容物酸化,从而增强对酸敏感病原体定植的抵抗力。应控制发酵程度以防止酸诱导的上皮细胞损伤。考虑到磷酸钙的缓冲能力及其肠道细胞保护作用,研究了补充磷酸钙是否会增强乳果糖发酵对肠道感染的抵抗力。
在一项严格控制的实验中,给大鼠喂食纯化的低钙对照饮食、低钙/乳果糖饮食或高钙/乳果糖饮食,随后经口感染肠炎沙门氏菌。
乳果糖发酵降低了肠道内容物的pH值并增加了乳酸浓度,这显著减少了该病原体在粪便中的排泄;因此提高了对定植的抵抗力。这与肠炎沙门氏菌在体外对乳酸(乳果糖发酵的主要代谢产物)的高敏感性一致。磷酸钙减少了肠炎沙门氏菌向体循环的易位,这一作用独立于乳果糖。补充磷酸钙可有效抵消乳果糖发酵导致的粪便水细胞毒性增加的不利影响。此外,从粪便中乳果糖排泄减少以及乳酸、氨和粪便氮排泄增加可以判断,磷酸钙刺激了乳果糖发酵。
在乳果糖饮食中添加额外的磷酸钙可提高对肠炎沙门氏菌定植和易位的抵抗力。这可能是由钙诱导的肠道微生物群对乳果糖发酵的刺激以及乳果糖介导的管腔细胞毒性增加的逆转介导的,从而减少了对肠黏膜的损伤。