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Article

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

by
Xiaoyue Li
1,2,3,
Zewen Liu
4,
Ting Gao
4,
Wei Liu
4,
Keli Yang
4,
Rui Guo
4,
Chang Li
4,
Yongxiang Tian
4,
Ningning Wang
1,
Danna Zhou
4,
Weicheng Bei
1,2,3,* and
Fangyan Yuan
4,*
1
National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
2
Cooperative Innovation Center of Sustainable Pig Production, Wuhan 430070, China
3
Hubei Hongshan Laboratory, Wuhan 430070, China
4
Key Laboratory of Prevention and Control Agents for Animal Bacteriosis (Ministry of Agriculture and Rural Affairs), Hubei Provincial Key Laboratory of Animal Pathogenic Microbiology, Institute of Animal Husbandry and Veterinary, Hubei Academy of Agricultural Sciences, Wuhan 430064, China
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2023, 24(14), 11842; https://doi.org/10.3390/ijms241411842
Submission received: 9 June 2023 / Revised: 13 July 2023 / Accepted: 18 July 2023 / Published: 24 July 2023
(This article belongs to the Special Issue Medicinal Plants and Natural Compounds in Health and Disease: Progresses, Challenges, Opportunities)
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Abstract

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 β-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-α. TP inhibited activation of the TLR/MAPK/PKC-MLCK signaling for down-regulated TLR-2, TLR4, p-JNK, p-p38, p-PKC-α, and MLCK in cells triggered by APP. Collectively, our data suggest that TP represents a promising therapeutic agent in the treatment of APP infection.
Keywords: tea polyphenols; Actinobacillus pleuropneumoniae; epithelial barrier; TLR-4/MAPK/PKC-MLCK signaling tea polyphenols; Actinobacillus pleuropneumoniae; epithelial barrier; TLR-4/MAPK/PKC-MLCK signaling

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MDPI and ACS Style

Li, X.; Liu, Z.; Gao, T.; Liu, W.; Yang, K.; Guo, R.; Li, C.; Tian, Y.; Wang, N.; Zhou, D.; et al. Tea Polyphenols Protects Tracheal Epithelial Tight Junctions in Lung during Actinobacillus pleuropneumoniae Infection via Suppressing TLR-4/MAPK/PKC-MLCK Signaling. Int. J. Mol. Sci. 2023, 24, 11842. https://doi.org/10.3390/ijms241411842

AMA Style

Li X, Liu Z, Gao T, Liu W, Yang K, Guo R, Li C, Tian Y, Wang N, Zhou D, et al. Tea Polyphenols Protects Tracheal Epithelial Tight Junctions in Lung during Actinobacillus pleuropneumoniae Infection via Suppressing TLR-4/MAPK/PKC-MLCK Signaling. International Journal of Molecular Sciences. 2023; 24(14):11842. https://doi.org/10.3390/ijms241411842

Chicago/Turabian Style

Li, Xiaoyue, Zewen Liu, Ting Gao, Wei Liu, Keli Yang, Rui Guo, Chang Li, Yongxiang Tian, Ningning Wang, Danna Zhou, and et al. 2023. "Tea Polyphenols Protects Tracheal Epithelial Tight Junctions in Lung during Actinobacillus pleuropneumoniae Infection via Suppressing TLR-4/MAPK/PKC-MLCK Signaling" International Journal of Molecular Sciences 24, no. 14: 11842. https://doi.org/10.3390/ijms241411842

APA Style

Li, X., Liu, Z., Gao, T., Liu, W., Yang, K., Guo, R., Li, C., Tian, Y., Wang, N., Zhou, D., Bei, W., & Yuan, F. (2023). Tea Polyphenols Protects Tracheal Epithelial Tight Junctions in Lung during Actinobacillus pleuropneumoniae Infection via Suppressing TLR-4/MAPK/PKC-MLCK Signaling. International Journal of Molecular Sciences, 24(14), 11842. https://doi.org/10.3390/ijms241411842

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