Evidence map›Paper›PMID 26676790›Full record

ArticleJournal of virology2015

Pulmonary C Fibers Modulate MMP-12 Production via PAR2 and Are Involved in the Long-Term Airway Inflammation and Airway Hyperresponsiveness Induced by Respiratory Syncytial Virus Infection.

Na Zang, Jianguo Zhuang, Yu Deng, Zhimei Yang, Zhixu Ye, Xiaohong Xie, Luo Ren, Zhou Fu, Zhengxiu Luo, Fadi Xu and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  7. Airway Resistance Caused by Sphingomyelin Synthase 2 Insufficiency in Response to Cigarette Smoke.American journal of respiratory cell and molecular biology · 2020
    Article
  8. Review
  9. Review
  10. NeonatalBioMed research international · 2019
    Article
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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

11 authors at 4 institutions in 2 countries.

Na ZangMinistry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing, China Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China Pathophysiology Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, USA.
Jianguo ZhuangPathophysiology Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, USA.
Yu DengDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China.
Zhimei YangDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China.
Zhixu YeMinistry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing, China.
Xiaohong XieDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China.
Luo RenMinistry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing, China.
Zhou FuDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China.
Zhengxiu LuoDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China.
Fadi XuPathophysiology Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, USA.
Enmei LiuDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China emliu186@hotmail.com.
Chongqing Medical University · CNLovelace Respiratory Research Institute · USChina International Science and Technology Cooperation · CNChildren's Hospital of Chongqing Medical University · CN

Funding

Lethal H5N1 Virus Infection and Respiratory DisordersR01HL119683 · NHLBI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI XU, FADI · 2013 to 2016
$2.1M
NHLBI NIH HHS R01 HL119683NHLBI NIH HHS R01 HL119683-01
6 · The paper itself

Abstract

unlabelledChildren with acute respiratory syncytial virus (RSV) infection often develop sequelae of persistent airway inflammation and wheezing. Pulmonary C fibers (PCFs) are involved in the generation of airway inflammation and resistance; however, their role in persistent airway diseases after RSV is unexplored. Here, we elucidated the pathogenesis of PCF activation in RSV-induced persistent airway disorders. PCF-degenerated and intact mice were used in the current study. Airway inflammation and airway resistance were evaluated. MMP408 and FSLLRY-NH2 were the selective antagonists for MMP-12 and PAR2, respectively, to investigate the roles of MMP-12 and PAR2 in PCFs mediating airway diseases. As a result, PCF degeneration significantly reduced the following responses to RSV infection: augmenting of inflammatory cells, especially macrophages, and infiltrating of inflammatory cells in lung tissues; specific airway resistance (sRaw) response to methacholine; and upregulation of MMP-12 and PAR2 expression. Moreover, the inhibition of MMP-12 reduced the total number of cells and macrophages in bronchiolar lavage fluid (BALF), as well infiltrating inflammatory cells, and decreased the sRaw response to methacholine. In addition, PAR2 was upregulated especially at the later stage of RSV infection. Downregulation of PAR2 ameliorated airway inflammation and resistance following RSV infection and suppressed the level of MMP-12. In all, the results suggest that PCF involvement in long-term airway inflammation and airway hyperresponsiveness occurred at least partially via modulating MMP-12, and the activation of PAR2 might be related to PCF-modulated MMP-12 production. Our initial findings indicated that the inhibition of PCF activity would be targeted therapeutically for virus infection-induced long-term airway disorders. IMPORTANCE: The current study is critical to understanding that PCFs are involved in long-term airway inflammation and airway resistance after RSV infection through mediating MMP-12 production via PAR2, indicating that the inhibition of PCF activity can be targeted therapeutically for virus infection-induced long-term airway disorders.

Indexed as

AnimalsDisease Models, AnimalFemaleInflammationLungMatrix Metalloproteinase 12Mice, Inbred BALB CNerve Fibers, UnmyelinatedReceptor, PAR-2Respiratory Syncytial Virus InfectionsMatrix Metalloproteinase 12Receptor, PAR-2

Identifiers

PMID26676790
PMCPMC4810725
OpenAlexW2208659894

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.