干酪乳杆菌对细菌性肠炎NF-κB通路及其介导的炎性介质的影响

Effects of Lactobacillus on the levels of the NF-κB and inflammatory mediators in the mouse inflammation model

为分析干酪乳杆菌(L.casei)对产肠毒素大肠杆菌(ETEC)K88引起的细菌性肠炎NF-kB信号通路及炎性介质的影响,本研究将90只BALB/c小鼠随机分成肠炎组(ETEC K88灌胃)、干预组(ETEC K88+L.casei灌胃)及对照组。对临床症状进行观察,利用荧光定量PCR方法检测肠系膜淋巴结中NF-κB、IL-1β及TNF-αm RNA水平,western blot方法检测肠系膜淋巴结中NF-κB蛋白表达量,ELISA方法检测外周血NO、PGE2含量。结果显示:肠炎组NF-κB、IL-1β、TNF-α mRNA表达水平、NF-κB蛋白表达量及NO、PGE2含量较高,与对照组相比差异显著(p<0.05)。经L.casei干预后,人工感染ETEC的小鼠临床症状好转,NF-κB、IL-1β、TNF-αm RNA表达水平、NF-κB蛋白表达量及NO、PGE2含量均显著下降(p<0.05)。表明L.casei可以通过抑制NF-κB的活化,降低IL-1β、TNF-α mRNA的表达,减少NO、PGE2的分泌,抑制肠道炎症的进一步发生。为L.casei的抑菌机制的深入研究奠定了基础。

The aim of this experiment was to investigate the pathogenesis of Lactobacillus casei on the enterotoxigenic Escherichia coli （ETEC） K88-induced NF-κB signaling pathway and inflammatory mediators of Bacterial enteritis. Ninety BALB/c mice were randomly assigned to the following groups： Control group, ETEC K88 group, and ETEC K88＋L.casei ATCC393 group. The clinical symptoms were observed. The mRNA levels of the NF-κB, IL-1β and TNF-α were detected using real-time PCR. The levels of the NF-κB protein were detected using western blot. The levels of NO and PEG2 were detected by ELISA. The results indicated that comparing to control group, the expression of TNF-α, IL-1β, NF-κB, NO, and PGE2 significantly increased in ETEC K88 group （p〈0.05）, and the expression of TNF-α, IL-1β, NF-κB, NO, and PGE2 in the ETEC K88 group were decreased in ETEC K88＋L.casei ATCC393 group （p〈0.05）. In conclusion, these data demonstrates that L.casei ATCC393 plays a protective role in ETEC K88-induced enteritis. L.casei ATCC393 possibly reduces ETEC K88-induced enteritis via NF-κB pathways, it inhibited the further development of intestinal inflammation. This study laid a foundation for further study on the antibacterial mechanism of L.casei.