Yu Qinghua, Yuan Lixia, Deng Jun, Yang Qian
College of Veterinary Medicine, Nanjing Agricultural University Nanjing, China.
Front Cell Infect Microbiol. 2015 Mar 25;5:26. doi: 10.3389/fcimb.2015.00026. eCollection 2015.
Pathogens invade intestinal mucosal barrier through phagocytosis of antigen presenting cells (dendritic cell, microfold cells), or through the invasion into the intestinal epithelial directly. Some pathogens could damage the cell junction between epithelial cells and use the paracellular pathway as an entrance to invade. Moreover, some Lactobacillus could inhibit the adhesion of the pathogens and protect the integrity of the cell junction and mucosal barrier. This research focused on the potential therapeutic effect of Lactobacillus fructosus (L. fructosus) C2 to attenuate ETEC K88 or S. typhimurium SL1344 induced changes to mucosal barrier. The results demonstrated that treatment of polarized Caco-2 cells with L. fructosus C2 reduced the permeation of dextran, and expression of IL-8, p-ERK, and p-JNK when cells were infected with pathogenic bacteria. The findings indicated that L. fructosus C2 exerted a protective effect against the damage to the integrity of Caco-2 cells by ETEC or S. typhimurium infection.
病原体通过抗原呈递细胞（树突状细胞、微褶细胞）的吞噬作用，或直接侵入肠上皮细胞来突破肠道黏膜屏障。一些病原体可破坏上皮细胞间的细胞连接，并利用细胞旁途径作为入侵入口。此外，一些乳酸杆菌可抑制病原体的黏附，并保护细胞连接和黏膜屏障的完整性。本研究聚焦于果糖乳酸杆菌（L. fructosus）C2对减轻肠毒素大肠杆菌K88或鼠伤寒沙门氏菌SL1344诱导的黏膜屏障变化的潜在治疗作用。结果表明，用果糖乳酸杆菌C2处理极化的Caco-2细胞，可降低葡聚糖的通透性，以及细胞感染病原菌时白细胞介素-8、磷酸化细胞外信号调节激酶和磷酸化应激活化蛋白激酶的表达。研究结果表明，果糖乳酸杆菌C2对肠毒素大肠杆菌或鼠伤寒沙门氏菌感染所致Caco-2细胞完整性损伤具有保护作用。
