Evidence map›Paper›PMID 33879121›Full record

ArticleRespiratory research2021

Long-term cigarette smoke exposure dysregulates pulmonary T cell response and IFN-γ protection to influenza virus in mouse.

Wenxin Wu, Lili Tian, Wei Zhang, J Leland Booth, Erola Ainsua-Enrich, Susan Kovats, Brent R Brown, Jordan P Metcalf

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

Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Cigarette smoke components modulate the MR1-MAIT axis.The Journal of experimental medicine · 2025
    Article
  3. Article
  4. Article
  5. 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

8 authors at 3 institutions in 1 country.

Wenxin WuPulmonary, Critical Care and Sleep Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Room 425, RP1, 800 N. Research Pkwy., Oklahoma City, OK, 73104, USA. Wenxin-Wu@ouhsc.edu.ORCID http://orcid.org/0000-0001-6333-6773
Lili TianPulmonary, Critical Care and Sleep Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Room 425, RP1, 800 N. Research Pkwy., Oklahoma City, OK, 73104, USA.
Wei ZhangPulmonary, Critical Care and Sleep Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Room 425, RP1, 800 N. Research Pkwy., Oklahoma City, OK, 73104, USA.
J Leland BoothPulmonary, Critical Care and Sleep Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Room 425, RP1, 800 N. Research Pkwy., Oklahoma City, OK, 73104, USA.
Erola Ainsua-EnrichArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Susan KovatsArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Brent R BrownPulmonary, Critical Care and Sleep Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Room 425, RP1, 800 N. Research Pkwy., Oklahoma City, OK, 73104, USA.
Jordan P MetcalfPulmonary, Critical Care and Sleep Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Room 425, RP1, 800 N. Research Pkwy., Oklahoma City, OK, 73104, USA. jordan-metcalf@ouhsc.edu.
University of Oklahoma Health Sciences Center · USOklahoma Medical Research Foundation · USVeterans Health Administration · US

Funding

Tracking and Evaluation CoreU54GM104938 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Valerie Williams · 2013 to 2026
$68.2M
ZFC3H1 Regulation of Host Defense and Influenza A Virus PathogenesisP20GM103648 · NIGMS · OKLAHOMA STATE UNIVERSITY STILLWATER · PI CHANNAPPANAVAR, RUDRAGOUDA · 2013 to 2022
$22.3M
OUHSC MOUSE FACILITIES IMPROVEMENT PROGRAMC06RR017598 · NCRR · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI WANER, JOSEPH L. · 2003 to 2003
$4.0M
IRF4-Mediated Regulation of Lung Dendritic Cells During Viral InfectionR01HL119501 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI KOVATS, SUSAN · 2014 to 2017
$1.7M
Reversing Cigarette Smoke-Induced Antiviral ImmunosuppressionI01BX005023 · VA · OKLAHOMA CITY VA MEDICAL CENTER · PI METCALF, JORDAN PATRICK · 2021 to 2024
–
BLRD VA I01 BX001937BLRD VA I01 BX005023NCRR NIH HHS C06 RR017598NHLBI NIH HHS 5R01HL119501NHLBI NIH HHS R01 HL119501NIGMS NIH HHS 5P20GM103648NIGMS NIH HHS P20 GM103648NIGMS NIH HHS U54 GM104938NIGMS NIH HHS U54GM104938
6 · The paper itself

Abstract

backgroundInfluenza is a highly contagious, acute, febrile respiratory infection caused by a negative-sense, single-stranded RNA virus, which belongs in the Orthomyxoviridae family. Cigarette smoke (CS) exposure worsens influenza infection in terms of frequency and severity in both human and animal models.

methodsC57BL/6 mice with or without CS exposure for 6 weeks were inoculated intranasally with a single, non-lethal dose of the influenza A virus (IAV) A/Puerto Rico/8/1934 (PR8) strain. At 7 and 10 days after infection, lung and mediastinal lymph nodes (MLN) cells were collected to determine the numbers of total CD4 + and CD8 + T cells, and IAV-specific CD4 + and CD8 + T cells, using flow cytometry. Bronchoalveolar lavage fluid (BALF) was also collected to determine IFN-γ levels and total protein concentration.

resultsAlthough long-term CS exposure suppressed early pulmonary IAV-antigen specific CD8 + and CD4 + T cell numbers and IFN-γ production in response to IAV infection on day 7 post-infection, CS enhanced numbers of these cells and IFN-γ production on day 10. The changes of total protein concentration in BALF are consistent with the changes in the IFN-γ amounts between day 7 and 10, which suggested that excessive IFN-γ impaired barrier function and caused lung injury at the later stage of infection.

conclusionsOur results demonstrated that prior CS exposure caused a biphasic T cell and IFN-γ response to subsequent infection with influenza in the lung. Specifically, the number of IAV antigen-specific T cells on day 10 was greatly increased by CS exposure even though CS decreased the number of the same group of cells on day 7. The result suggested that CS affected the kinetics of the T cell response to IAV, which was suppressed at an early stage and exaggerated at a later stage. This study is the first to describe the different effect of long-term CS on T cell responses to IAV at early and late stages of infection in vivo.

Indexed as

Lymphocyte ActivationAnimalsDisease Models, AnimalFemaleHost-Pathogen InteractionsInfluenza A Virus, H1N1 SubtypeInterferon-gammaLungMaleMiceMice, Inbred C57BLOrthomyxoviridae InfectionsSmokeTime FactorsT-LymphocytesTobacco ProductsIFNG protein, mouseInterferon-gammaSmokeCigarette smokeCTLIFN-γInfluenzaT lymphocyteVirus

Identifiers

PMID33879121
PMCPMC8056367
OpenAlexW3153505947

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.