Evidence map›Paper›PMID 26001778›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015

Influenza-induced type I interferon enhances susceptibility to gram-negative and gram-positive bacterial pneumonia in mice.

Benjamin Lee, Keven M Robinson, Kevin J McHugh, Erich V Scheller, Sivanarayana Mandalapu, Chen Chen, Y Peter Di, Michelle E Clay, Richard I Enelow, Patricia J Dubin and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

92 citing papers in PubMed, 129 citations in OpenAlex.

  1. Myeloid cell reprogramming drives enhanced defense againstProceedings of the National Academy of Sciences of the United States of America · 2026
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  8. (Inter)feron the Reaper: New Insights on an Old Cytokine in Secondary Bacterial Pneumonia.American journal of respiratory cell and molecular biology · 2025
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  19. A Fatal Case ofMicroorganisms · 2023
    Review
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32 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 1 country.

Benjamin LeeDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania;
Keven M RobinsonDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania; Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania;
Kevin J McHughDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania;
Erich V SchellerDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania;
Sivanarayana MandalapuDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania;
Chen ChenDepartment of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania; and.
Y Peter DiDepartment of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania; and.
Michelle E ClayDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania;
Richard I EnelowDepartment of Medicine, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire.ORCID http://orcid.org/0000-0003-2759-3929
Patricia J DubinDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania;
John F AlcornDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania; john.alcorn@chp.edu.
Children's Hospital of Pittsburgh · USUniversity of Pittsburgh · USDartmouth College · US

Funding

Translational Training Program in Pulmonary Biology and MedicineT32HL007563 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Melanie Koenigshoff · 1985 to 2026
$12.3M
Influenza A Inhibits TH17 Host Defense Against Bacterial PneumoniaR01HL107380 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ALCORN, JOHN F · 2012 to 2024
$5.4M
Research Training Program for Pediatric Subspecialty FellowsT32HD071834 · NICHD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TERENCE S. DERMODY · 2013 to 2026
$4.7M
Epithelial PLUNC as a determinant of Airway Mucosal Antimicrobial ActivityR01HL091938 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DI, YUANPU PETER · 2008 to 2012
$2.3M
NHLBI NIH HHS R01 HL091938NHLBI NIH HHS R01 HL107380NHLBI NIH HHS T32 HL007563NICHD NIH HHS T32 HD071834
6 · The paper itself

Abstract

Suppression of type 17 immunity by type I interferon (IFN) during influenza A infection has been shown to enhance susceptibility to secondary bacterial pneumonia. Although this mechanism has been described in coinfection with gram-positive bacteria, it is unclear whether similar mechanisms may impair lung defense against gram-negative infections. Furthermore, precise delineation of the duration of type I IFN-associated susceptibility to bacterial infection remains underexplored. Therefore, we investigated the effects of preceding influenza A virus infection on subsequent challenge with the gram-negative bacteria Escherichia coli or Pseudomonas aeruginosa and the temporal association between IFN expression with susceptibility to Staphylococcus aureus challenge in a mouse model of influenza and bacterial coinfection. Here we demonstrate that preceding influenza A virus led to increased lung E. coli and P. aeruginosa bacterial burden, which was associated with suppression of type 17 immunity and attenuation of antimicrobial peptide expression. Enhanced susceptibility to S. aureus coinfection ceased at day 14 of influenza infection, when influenza-associated type I IFN levels had returned to baseline levels, further suggesting a key role for type I IFN in coinfection pathogenesis. These findings further implicate type I IFN-associated suppression of type 17 immunity and antimicrobial peptide production as a conserved mechanism for enhanced susceptibility to both gram-positive and gram-negative bacterial coinfection during influenza infection.

Indexed as

AnimalsAntimicrobial Cationic PeptidesCoinfectionDisease SusceptibilityEscherichia coliEscherichia coli InfectionsInfluenza A virusMaleMiceMice, Inbred C57BLMice, KnockoutOrthomyxoviridae InfectionsPneumoniaPneumonia, BacterialReceptor, Interferon alpha-betaStaphylococcal InfectionsAntimicrobial Cationic PeptidesIfnar1 protein, mouseReceptor, Interferon alpha-betacoinfectionEscherichia coliinfluenza AStaphylococcus aureustype I interferon

Identifiers

PMID26001778
PMCPMC4504975
OpenAlexW2301738150

What OpenQuestion holds

Textmetadata
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.