Hypothetical protein Cpn0423 triggers NOD2 activation and contributes to Chlamydia pneumoniae-mediated inflammationReportar como inadecuado

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BMC Microbiology

, 17:153

Signaling and cellular microbiology


BackgroundChlamydia 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.

ResultsCpn0423 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.

ConclusionCpn0423 could be sensed by NOD2, which was identified as an essential element in a pathway contributing to the development of C. pneumoniae -mediated inflammation.

KeywordsChlamydia pneumoniae Cpn0423 NOD2 Inflammatory AbbreviationsBALFBronchoalveolar lavage fluid

BMDMbone marrow-derived macrophages

CpnChlamydia pneumoniae


MDPmuramyl dipeptide

MIP-2macrophage inflammatory protein-2

NOD2Nucleotide-binding oligomerization domain-containing protein 2

NOD2-Con-siRNAsmall interfering RNA negative control for NOD2

NOD2-siRNAsmall interfering RNA against NOD2


TLRToll-like receptors

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Autor: Hong-liang Chen - Guo-zhi Dai - An-wen Zhou - Ran-hui Li - Hong-xia Yuan - Jing Xiang - Xiao-xing You - Ou Ran - Yi-mou W

Fuente: https://link.springer.com/

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