Evidence map›Paper›PMID 36341376›Full record

ReviewFrontiers in immunology2022

Alveolar macrophages and airway hyperresponsiveness associated with respiratory syncytial virus infection.

Yuxin Wang, Junwen Zheng, Xia Wang, Pu Yang, Dongchi Zhao

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
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  4. Suppression of Nr1d1/Bnip3-dependent mitophagy by notch signaling aggravates inflammatory response in RSV-infected mice lungs.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
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  7. Article
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  11. Article
  12. Article
  13. Review
  14. Article
  15. Analysis of BeyfortusCurrent issues in molecular biology · 2024
    Review
  16. Article
  17. Cholinergic Polarization of Human Macrophages.International journal of molecular sciences · 2023
    Review
  18. Review
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  20. Review
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

5 authors at 2 institutions in 1 country.

Yuxin WangDepartment of Pediatrics, Zhongnan Hospital of Wuhan University, Wuhan, China.
Junwen ZhengDepartment of Pediatrics, Zhongnan Hospital of Wuhan University, Wuhan, China.
Xia WangDepartment of Pediatrics, Zhongnan Hospital of Wuhan University, Wuhan, China.
Pu YangDepartment of Pediatrics, Zhongnan Hospital of Wuhan University, Wuhan, China.
Dongchi ZhaoDepartment of Pediatrics, Zhongnan Hospital of Wuhan University, Wuhan, China.
Wuhan University · CNZhongnan Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is a ubiquitous pathogen of viral bronchiolitis and pneumonia in children younger than 2 years of age, which is closely associated with recurrent wheezing and airway hyperresponsiveness (AHR). Alveolar macrophages (AMs) located on the surface of the alveoli cavity are the important innate immune barrier in the respiratory tract. AMs are recognized as recruited airspace macrophages (RecAMs) and resident airspace macrophages (RAMs) based on their origins and roaming traits. AMs are polarized in the case of RSV infection, forming two macrophage phenotypes termed as M1-like and M2-like macrophages. Both M1 macrophages and M2 macrophages are involved in the modulation of inflammatory responses, among which M1 macrophages are capable of pro-inflammatory responses and M2 macrophages are capable of anti-proinflammatory responses and repair damaged tissues in the acute and convalescent phases of RSV infection. Polarized AMs affect disease progression through the alteration of immune cell surface phenotypes as well as participate in the regulation of T lymphocyte differentiation and the type of inflammatory response, which are closely associated with long-term AHR. In recent years, some progress have been made in the regulatory mechanism of AM polarization caused by RSV infection, which participates in acute respiratory inflammatory response and mediating AHR in infants. Here we summarized the role of RSV-infection-mediated AM polarization associated with AHR in infants.

Indexed as

PneumoniaRespiratory HypersensitivityRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsHumansInflammationMacrophages, Alveolarairway hyperresponsivenessalveolar macrophagesimmune regulationpolarizationrespiratory syncytial virus

Identifiers

PMID36341376
PMCPMC9630648
OpenAlexW4306946090

What OpenQuestion holds

Textmetadata
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.