Evidence map›Paper›PMID 28693414›Full record

ArticleBMC microbiology2017

Hypothetical protein Cpn0423 triggers NOD2 activation and contributes to Chlamydia pneumoniae-mediated inflammation.

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

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 93% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Frontiers in cellular and infection microbiology · 2026
    Review
  2. Alterations of Vaginal Microbiota in Women With Infertility andFrontiers in cellular and infection microbiology · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Hong-Liang ChenDepartment of Clinical Laboratory, ChenZhou NO.1 People's Hospital, ChenZhou, 423000, China.
Guo-Zhi DaiDepartment of Clinical Laboratory, ChenZhou NO.1 People's Hospital, ChenZhou, 423000, China.
An-Wen ZhouDepartment of Clinical Laboratory, ChenZhou NO.1 People's Hospital, ChenZhou, 423000, China.
Ran-Hui LiInstitute of Pathogenic Biology, Medical College, University of South China, Hengyang, 421001, China.
Hong-Xia YuanDepartment of Clinical Laboratory, ChenZhou NO.1 People's Hospital, ChenZhou, 423000, China.
Jing XiangDepartment of Clinical Laboratory, ChenZhou NO.1 People's Hospital, ChenZhou, 423000, China.
Xiao-Xing YouInstitute of Pathogenic Biology, Medical College, University of South China, Hengyang, 421001, China.
Ou RanInstitute of Pathogenic Biology, Medical College, University of South China, Hengyang, 421001, China.
Yi-Mou WuInstitute of Pathogenic Biology, Medical College, University of South China, Hengyang, 421001, China. yimouwu@sina.com.ORCID http://orcid.org/0000-0001-6883-1677
Chenzhou First People's Hospital · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AnimalsBacterial ProteinsChemokine CXCL2Chlamydophila InfectionsChlamydophila pneumoniaeHumansInflammation MediatorsInterleukinsLungMaleMiceMice, Inbred C57BLNod2 Signaling Adaptor ProteinPneumonia, BacterialBacterial ProteinsChemokine CXCL2Inflammation MediatorsInterleukinsNod2 protein, mouseNod2 Signaling Adaptor ProteinChlamydia pneumoniaeCpn0423InflammatoryNOD2

Identifiers

PMID28693414
PMCPMC5504769
OpenAlexW2735859307

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.