Evidence map›Paper›PMID 21939519›Full record

ArticleRespiratory research2011

Attenuation of antigen-induced airway hyperresponsiveness and inflammation in CXCR3 knockout mice.

Yi Lin, Haibo Yan, Yu Xiao, Hongmei Piao, Ruolan Xiang, Lei Jiang, Huaxia Chen, Kewu Huang, Zijian Guo, Wexun Zhou and 2 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Respiratory research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Dual role for CXCR3 and CCR5 in asthmatic type 1 inflammation.The Journal of allergy and clinical immunology · 2022
    Article
  5. Article
  6. Article
  7. Critical Role of IRAK-M in Regulating Antigen-Induced Airway Inflammation.American journal of respiratory cell and molecular biology · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. ORMDL3 is an inducible lung epithelial gene regulating metalloproteases, chemokines, OAS, and ATF6.Proceedings of the National Academy of Sciences of the United States of America · 2012
    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

12 authors at 7 institutions in 2 countries.

Yi LinDepartment of Respiratory Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
Haibo Yan
Yu Xiao
Hongmei Piao
Ruolan Xiang
Lei Jiang
Huaxia Chen
Kewu Huang
Zijian Guo
Wexun Zhou
Bao Lu
Jinming Gao
Peking Union Medical College Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNBeijing Chao-Yang Hospital · CNHarvard University · USPeking University · CNYanbian University · CNYanbian University Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD8+ T cells participate in airway hyperresponsiveness (AHR) and allergic pulmonary inflammation that are characteristics of asthma. CXCL10 by binding to CXCR3 expressed preferentially on activated CD8+ T cells, attracts T cells homing to the lung. We studied the contribution and limitation of CXCR3 to AHR and airway inflammation induced by ovalbumin (OVA) using CXCR3 knockout (KO) mice.

methodsMice were sensitized and challenged with OVA. Lung histopathological changes, AHR, cellular composition and levels of inflammatory mediators in bronchoalveolar lavage (BAL) fluid, and lungs at mRNA and protein levels, were compared between CXCR3 KO mice and wild type (WT) mice.

resultsCompared with the WT controls, CXCR3 KO mice showed less OVA-induced infiltration of inflammatory cells around airways and vessels, and less mucus production. CXCR3 KO mice failed to develop significant AHR. They also demonstrated significantly fewer CD8+ T and CD4+ T cells in BAL fluid, lower levels of TNFα and IL-4 in lung tissue measured by real-time RT-PCR and in BAL fluid by ELISA, with significant elevation of IFNγ mRNA and protein expression levels.

conclusionsWe conclude that CXCR3 is crucial for AHR and airway inflammation by promoting recruitment of more CD8+ T cells, as well as CD4+ T cells, and initiating release of proinflammatory mediators following OVA sensitization and challenge. CXCR3 may represent a novel therapeutic target for asthma.

Indexed as

AnimalsAntigensBronchial HyperreactivityCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesFemaleInflammation MediatorsMaleMiceMice, Inbred C57BLMice, KnockoutOvalbuminReceptors, CXCR3AntigensCxcr3 protein, mouseInflammation MediatorsOvalbuminReceptors, CXCR3

Identifiers

PMID21939519
PMCPMC3199245
OpenAlexW2149415013

What OpenQuestion holds

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LicenceCC BY
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.