Evidence map›Paper›PMID 24889245›Full record

ArticleVirology2014

IL-17 contributes to neutrophil recruitment but not to control of viral replication during acute mouse adenovirus type 1 respiratory infection.

Mary K McCarthy, Lingqiao Zhu, Megan C Procario, Jason B Weinberg

Open access · greenAbstract read
In one paragraph

Article in Virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. A Review of the Safety of Interleukin-17A Inhibitor Secukinumab.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
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  6. Article
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  10. Article
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  13. Article
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  15. Article
  16. Article
  17. Article
  18. Expression of IL-17 and syndecan-1 in nasal polyps and their correlation with nasal polyps.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017
    Article
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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

4 authors at 1 institution in 1 country.

Mary K McCarthyDepartment of Microbiology and Immunology, University of Michigan, 5641 Medical Science Building II, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA. Electronic address: mkmccar@umich.edu.
Lingqiao ZhuDepartment of Microbiology and Immunology, University of Michigan, 5641 Medical Science Building II, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA. Electronic address: lingqiao.zhu@gmail.com.
Megan C ProcarioDepartment of Pediatrics and Communicable Diseases, University of Michigan, 7510A Medical Science Research Building I, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA. Electronic address: mcprocar@umich.edu.
Jason B WeinbergDepartment of Microbiology and Immunology, University of Michigan, 5641 Medical Science Building II, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA; Department of Pediatrics and Communicable Diseases, University of Michigan, 7510A Medical Science Research Building I, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA. Electronic address: jbwein@umich.edu.
University of Michigan · US

Funding

Modulation of adenovirus pathogenesis by prostaglandin E2R01AI083334 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WEINBERG, JASON BRICE · 2010 to 2014
$1.9M
NIAID NIH HHS R01 AI083334NIAID NIH HHS R01AI083334
6 · The paper itself

Abstract

IL-17-producing CD4(+) helper T cells (Th17 cells) promote inflammatory responses to many pathogens. We used mouse adenovirus type 1 (MAV-1) to determine contributions of IL-17 to adenovirus pathogenesis. MAV-1 infection of C57BL/6 mice upregulated lung expression of IL-17 and the Th17-associated factors IL-23 and RORγt. Only CD4(+)T cells were associated with virus-specific IL-17 production. Fewer neutrophils were recruited to airways of IL-17(-/-) mice following MAV-1 infection, but there were no other differences in pulmonary inflammation between IL-17(+/+) and IL-17(-/-) mice. Mice depleted of neutrophils using anti-Gr-1 antibody had greater lung viral loads than controls. Despite impaired neutrophil recruitment, there were no differences between IL-17(+/+) and IL-17(-/-) mice in peak lung viral loads, clearance of virus from the lungs, or establishment of protective immunity. We demonstrate robust Th17 responses during MAV-1 respiratory infection, but these responses are not essential for control of virus infection or for virus-induced pulmonary inflammation.

Indexed as

Host-Pathogen InteractionsNeutrophil InfiltrationVirus ReplicationAdenoviridaeAdenoviridae InfectionsAnimalsCD4-Positive T-LymphocytesDisease Models, AnimalHumansInterleukin-17MiceMice, Inbred C57BLMice, KnockoutRespiratory Tract InfectionsInterleukin-17AdenovirusIL-17Rspiratory infectionTh17

Identifiers

PMID24889245
PMCPMC4048921
OpenAlexW2086853941

What OpenQuestion holds

Textmetadata
LicenceTDM
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.