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Capsular Polysaccharide is a Main Component of Mycoplasma ovipneumoniae in the Pathogen-Induced Toll-Like Receptor-Mediated Inflammatory Responses in Sheep Airway Epithelial Cells
Journal article   Open access   Peer reviewed

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

Zhongjia Jiang, Fuyang Song, Yanan Li, Di Xue, Guangcun Deng, Min Li, Xiaoming Liu and Yujiong Wang
Mediators of inflammation, Vol.2017, pp.9891673-9891673
2017
DOI: 10.1155/2017/9891673
PMCID: PMC5434471
PMID: 28553017
url
https://doi.org/10.1155/2017/9891673View
Published (Version of record) Open Access

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.
Bronchi - microbiology Epithelial Cells - metabolism Cytokines - metabolism Enzyme-Linked Immunosorbent Assay Signal Transduction Bacterial Capsules - metabolism Cells, Cultured Pneumonia, Mycoplasma - microbiology Polysaccharides, Bacterial - metabolism Respiratory System NF-kappa B - metabolism Pneumonia, Mycoplasma - veterinary Transcription Factor AP-1 - metabolism Host-Pathogen Interactions Inflammation - metabolism Animals Epithelial Cells - microbiology Sheep Toll-Like Receptors - metabolism Mycoplasma ovipneumoniae Myeloid Differentiation Factor 88 - metabolism

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