Evidence map›Paper›PMID 27354786›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2016

α1-Antitrypsin reduces rhinovirus infection in primary human airway epithelial cells exposed to cigarette smoke.

Reena Berman, Di Jiang, Qun Wu, Hong Wei Chu

Open access · goldAbstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2016. 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
4.0field-weighted citation impact, top 7% 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, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Rhinovirus and Innate Immune Function of Airway Epithelium.Frontiers in cellular and infection microbiology · 2020
    Review
  11. Article
  12. Article
  13. Rhinovirus and COPD airway epithelium.Pulmonary and critical care medicine · 2017
    Article
  14. 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

4 authors at 2 institutions in 1 country.

Reena BermanDepartment of Medicine, National Jewish Health, Denver, CO, USA.
Di JiangDepartment of Medicine, National Jewish Health, Denver, CO, USA.
Qun WuDepartment of Medicine, National Jewish Health, Denver, CO, USA.
Hong Wei ChuDepartment of Medicine, National Jewish Health, Denver, CO, USA.
National Jewish Health · USUniversity of Colorado Denver · US

Funding

IRAK-M in lung defense against rhinovirus infectionR01AI106287 · NIAID · NATIONAL JEWISH HEALTH · PI CHU, HONG W, LI, LIWU · 2014 to 2018
$2.0M
Novel function of MUC18: amplification of inflammation in allergic lungsR01HL122321 · NHLBI · NATIONAL JEWISH HEALTH · PI CHU, HONG W · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL122321NIAID NIH HHS R01 AI106287
6 · The paper itself

Abstract

Human rhinovirus (HRV) infections target airway epithelium and are the leading cause of acute exacerbations of COPD. Cigarette smoke (CS) increases the severity of viral infections, but there is no effective therapy for HRV infection. We determined whether α1-antitrypsin (A1AT) reduces HRV-16 infection in CS-exposed primary human airway epithelial cells. Brushed bronchial epithelial cells from normal subjects and patients diagnosed with COPD were cultured at air-liquid interface to induce mucociliary differentiation. These cells were treated with A1AT or bovine serum albumin for 2 hours and then exposed to air or whole cigarette smoke (WCS) with or without HRV-16 (5×10(4) 50% Tissue Culture Infective Dose [TCID50]/transwell) infection for 24 hours. WCS exposure significantly increased viral load by an average of fivefold and decreased the expression of antiviral genes interferon-λ1, OAS1, and MX1. When A1AT was added to WCS-exposed cells, viral load significantly decreased by an average of 29-fold. HRV-16 infection significantly increased HRV-16 receptor intercellular adhesion molecule-1 messenger RNA expression in air-exposed cells, which was decreased by A1AT. A1AT-mediated reduction of viral load was not accompanied by increased epithelial antiviral gene expression or by inhibiting the activity of 3C protease involved in viral replication or maturation. Our findings demonstrate that A1AT treatment prevents a WCS-induced increase in viral load and for the first time suggest a therapeutic effect of A1AT on HRV infection.

Indexed as

Agedalpha 1-AntitrypsinAntiviral AgentsBronchiCase-Control StudiesCells, CulturedEpithelial CellsFemaleHost-Pathogen InteractionsHumansIntercellular Adhesion Molecule-1MaleMiddle AgedPicornaviridae InfectionsPulmonary Disease, Chronic ObstructiveRespiratory Mucosaalpha 1-AntitrypsinAntiviral AgentsICAM1 protein, humanIntercellular Adhesion Molecule-1Smokecigarette smokeCOPDICAM-1rhinovirusα1-antitrypsin

Identifiers

PMID27354786
PMCPMC4910614
OpenAlexW2410443362

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.