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益生菌通过诱导肠道黏蛋白基因表达在体外抑制肠道致病性大肠杆菌的黏附。

Probiotics inhibit enteropathogenic E. coli adherence in vitro by inducing intestinal mucin gene expression.

作者信息

Mack D R, Michail S, Wei S, McDougall L, Hollingsworth M A

机构信息

Combined Section of Pediatric Gastroenterology and Nutrition, Department of Pediatrics, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA.

出版信息

Am J Physiol. 1999 Apr;276(4):G941-50. doi: 10.1152/ajpgi.1999.276.4.G941.

DOI:10.1152/ajpgi.1999.276.4.G941
PMID:10198338
Abstract

Probiotic agents, live microorganisms with beneficial effects for the host, may offer an alternative to conventional antimicrobials in the treatment and prevention of enteric infections. The probiotic agents Lactobacillus plantarum 299v and Lactobacillus rhamnosus GG quantitatively inhibited the adherence of an attaching and effacing pathogenic Escherichia coli to HT-29 intestinal epithelial cells but did not inhibit adherence to nonintestinal HEp-2 cells. HT-29 cells were grown under conditions that induced high levels of either MUC2 or MUC3 mRNA, but HEp-2 cells expressed only minimal levels of MUC2 and no MUC3 mRNA. Media enriched for MUC2 and MUC3 mucin were added exogenously to binding assays and were shown to be capable of inhibiting enteropathogen adherence to HEp-2 cells. Incubation of L. plantarum 299v with HT-29 cells increased MUC2 and MUC3 mRNA expression levels. From these in vitro studies, we propose the hypothesis that the ability of probiotic agents to inhibit adherence of attaching and effacing organisms to intestinal epithelial cells is mediated through their ability to increase expression of MUC2 and MUC3 intestinal mucins.

摘要

益生菌制剂是对宿主有有益作用的活微生物,在治疗和预防肠道感染方面可能是传统抗菌药物的一种替代选择。植物乳杆菌299v和鼠李糖乳杆菌GG这两种益生菌制剂可定量抑制黏附和损伤性致病性大肠杆菌对HT - 29肠上皮细胞的黏附,但不抑制其对非肠道HEp - 2细胞的黏附。HT - 29细胞在诱导MUC2或MUC3 mRNA高水平表达的条件下生长,但HEp - 2细胞仅表达极低水平的MUC2且不表达MUC3 mRNA。在黏附试验中,向培养基中外源添加富含MUC2和MUC3黏蛋白的物质,结果显示其能够抑制肠道病原体对HEp - 2细胞的黏附。植物乳杆菌299v与HT - 29细胞共孵育可提高MUC2和MUC3 mRNA的表达水平。基于这些体外研究,我们提出如下假说:益生菌制剂抑制黏附和损伤性微生物对肠上皮细胞黏附的能力是通过其增加MUC2和MUC3肠道黏蛋白表达的能力介导的。

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