Hypothetical Protein Cpn0423 Triggers NOD2 Activation and Contributes to Chlamydia Pneumoniae-mediated Inflammation

Overview

Journal BMC Microbiol

Publisher Biomed Central

Specialty Microbiology

Date 2017 Jul 12

PMID 28693414

Citations 1

Authors

Hong-Liang Chen

Guo-Zhi Dai

An-Wen Zhou

Ran-Hui Li

Hong-Xia Yuan

Jing Xiang

Xiao-Xing You

Ou Ran

Yi-Mou Wu

Affiliations

Soon will be listed here.

Abstract

Background: Chlamydia pneumoniae (C. pneumoniae) is pathogenic to humans, by causing pulmonary inflammation or bronchitis in both adolescents and young adults. However, the molecular signals linking C. pneumoniae components to inflammation remain elusive. This study was to investigate the effect of Chlamydia-specific Cpn0423 of C. pneumoniae on C. pneumoniae-mediated inflammation.

Results: Cpn0423 was detected outside of C. pneumoniae inclusions, which induced production of several cytokines including macrophage inflammatory protein-2 (MIP-2) and interleukins (ILs). Production of the Cpn0423-induced cytokines was markedly reduced in cells pretreated with NOD2-siRNA, but not with negative control oligonucleotides. Mice treated with Cpn0423 through intranasal administration exhibited pulmonary inflammation as evidenced by infiltration of inflammatory cells, increased inflammatory scores in the lung histology, recruitment of neutrophils and increased cytokines levels in the BALF.

Conclusion: Cpn0423 could be sensed by NOD2, which was identified as an essential element in a pathway contributing to the development of C. pneumoniae -mediated inflammation.

Citing Articles

Alterations of Vaginal Microbiota in Women With Infertility and Infection.

Chen H, Wang L, Zhao L, Luo L, Min S, Wen Y Front Cell Infect Microbiol. 2021; 11:698840.

PMID: 34414130 PMC: 8370387. DOI: 10.3389/fcimb.2021.698840.

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