Capsular Polysaccharide is a Main Component of in the Pathogen-Induced Toll-Like Receptor-Mediated Inflammatory Responses in Sheep Airway Epithelial Cells

Overview

Journal Mediators Inflamm

Publisher Wiley

Specialties Biochemistry
Pathology

Date 2017 May 30

PMID 28553017

Citations 13

Authors

Zhongjia Jiang

Fuyang Song

Yanan Li

Di Xue

Guangcun Deng

Min Li

Xiaoming Liu

Yujiong Wang

Affiliations

Soon will be listed here.

Abstract

() is characterized as an etiological agent of primary atypical pneumonia that specifically infects sheep and goat. In an attempt to better understand the pathogen-host interaction between the invading and airway epithelial cells, we investigated the host inflammatory responses against capsular polysaccharide (designated as CPS) of using sheep bronchial epithelial cells cultured in an air-liquid interface (ALI) model. Results showed that CPS derived from could activate toll-like receptor- (TLR-) mediated inflammatory responses, along with an elevated expression of nuclear factor kappa B (NF-B), activator protein-1 (AP-1), and interferon regulatory factor 3 (IRF3) as well as various inflammatory-associated mediators, representatively including proinflammatory cytokines, such as IL1, TNF, and IL8, and anti-inflammatory cytokines such as IL10 and TGF of TLR signaling cascade. Mechanistically, the CPS-induced inflammation was TLR initiated and was mediated by activations of both MyD88-dependent and MyD88-independent signaling pathways. Of importance, a blockage of CPS with specific antibody led a significant reduction of -induced inflammatory responses in sheep bronchial epithelial cells. These results suggested that CPS is a key virulent component of , which may play a crucial role in the inflammatory response induced by infections.

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