Tea Polyphenols Protects Tracheal Epithelial Tight Junctions in Lung during Actinobacillus pleuropneumoniae Infection via Suppressing TLR-4/MAPK/PKC-MLCK Signaling

文献类型： 外文期刊

第一作者： Li, Xiaoyue

作者： Li, Xiaoyue;Wang, Ningning;Bei, Weicheng;Li, Xiaoyue;Bei, Weicheng;Li, Xiaoyue;Bei, Weicheng;Liu, Zewen;Gao, Ting;Liu, Wei;Yang, Keli;Guo, Rui;Li, Chang;Tian, Yongxiang;Zhou, Danna;Yuan, Fangyan

作者机构：

关键词： tea polyphenols; Actinobacillus pleuropneumoniae; epithelial barrier; TLR-4; MAPK; PKC-MLCK signaling

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：5.6； 五年影响因子：6.2 ）

ISSN： 1661-6596

年卷期： 2023 年 24 卷 14 期

页码：

收录情况： SCI

摘要： Actinobacillus pleuropneumoniae (APP) is the causative pathogen of porcine pleuropneumonia, a highly contagious respiratory disease in the pig industry. The increasingly severe antimicrobial resistance in APP urgently requires novel antibacterial alternatives for the treatment of APP infection. In this study, we investigated the effect of tea polyphenols (TP) against APP. MIC and MBC of TP showed significant inhibitory effects on bacteria growth and caused cellular damage to APP. Furthermore, TP decreased adherent activity of APP to the newborn pig tracheal epithelial cells (NPTr) and the destruction of the tight adherence junction proteins & beta;-catenin and occludin. Moreover, TP improved the survival rate of APP infected mice but also attenuated the release of the inflammation-related cytokines IL-6, IL-8, and TNF-& alpha;. TP inhibited activation of the TLR/MAPK/PKC-MLCK signaling for down-regulated TLR-2, TLR4, p-JNK, p-p38, p-PKC-& alpha;, and MLCK in cells triggered by APP. Collectively, our data suggest that TP represents a promising therapeutic agent in the treatment of APP infection.

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