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Immunomodulatory effects of Lactobacillus plantarum on human colon cancer cells

植物乳杆菌 β防御素 微生物学 分泌物 抗菌肽 生物 免疫系统 先天免疫系统 致病菌 抗菌剂 抗体 细菌 免疫学 生物化学 乳酸 遗传学
作者
Rossella Paolillo,Caterina Romano Carratelli,Sabato Sorrentino,Nello Mazzola,Antonietta Rizzo
出处
期刊:International Immunopharmacology [Elsevier BV]
卷期号:9 (11): 1265-1271 被引量:104
标识
DOI:10.1016/j.intimp.2009.07.008
摘要

Probiotics, defined as live microbial food supplements which improve the health of the host, have obtained increasing medical importance. In the intestine they may prevent the overgrowth of pathogenic bacteria, increase the resistance of the gut to invasion by pathogens and ameliorate disease processes by inducting the secretion of soluble factors such as cytokines and antimicrobial beta-peptides. One important class of human antimicrobial peptides is the family of defensins. Human beta-defensin 2 (HBD-2) is a major inducible peptide which plays an important role in host defense and represents a link between innate and adaptive immune responses. This linkage is in part mediated through the recognition of conserved bacterial products or bacteria by Toll-like receptors (TLRs). The aim of this study was to investigate the effects of Lactobacillus plantarum on intestinal epithelial cells. We found that Caco-2 cells exposed to L. plantarum bacteria significantly induced HBD-2 mRNA expression and HBD-2 secretion in a dose- (16+/-1.4 pg/ml and 31.5+/-2.3 pg/ml at MOI 10 and 50, respectively) and time-dependent manner, but not HBD-3, compared to controls; in addition, when LPS was added to cells for 48 h, the interleukin (IL)-23 secretion (850+/-5.4 pg/ml) and IL-23 mRNA expression increased; while it was reduced when LPS was cocultured with L. plantarum (330+/-4.2 pg/ml). The L. plantarum-induced increase in HBD-2 expression is inhibited by anti-TLR-2 neutralizing antibodies, in the same way the pre-treatment with the anti-TLR-2 antibody inhibited the production of IL-23 induced by LPS in Caco-2 cells. The results of our study help to achieve a better understanding of how the intestinal epithelium participates in the innate immune response to commensal bacteria and pathogens in the gut.

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