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2017 ; 17
(1
): 153
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Hypothetical protein Cpn0423 triggers NOD2 activation and contributes to
Chlamydia pneumoniae-mediated inflammation
#MMPMID28693414
Chen HL
; Dai GZ
; Zhou AW
; Li RH
; Yuan HX
; Xiang J
; You XX
; Ran O
; Wu YM
BMC Microbiol
2017[Jul]; 17
(1
): 153
PMID28693414
show ga
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.