Evidence map›Paper›PMID 26015944›Full record

ArticleMolecular therapy. Methods & clinical development2014

Type 1 interferon gene transfer enhances host defense against pulmonary Streptococcus pneumoniae infection via activating innate leukocytes.

Daniela Damjanovic, Amandeep Khera, Maria Fe Medina, Jane Ennis, Jeffrey D Turner, Jack Gauldie, Zhou Xing

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Methods & clinical development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 30 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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  3. Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026
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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

7 authors at 2 institutions in 1 country.

Daniela DamjanovicMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University , Hamilton, Ontario, Canada ; M.G. DeGroote Institute for Infectious Disease Research, McMaster University , Hamilton, Ontario, Canada.
Amandeep KheraMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University , Hamilton, Ontario, Canada ; M.G. DeGroote Institute for Infectious Disease Research, McMaster University , Hamilton, Ontario, Canada.
Maria Fe MedinaMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University , Hamilton, Ontario, Canada ; M.G. DeGroote Institute for Infectious Disease Research, McMaster University , Hamilton, Ontario, Canada.
Jane EnnisDefyrus , Toronto, Ontario, Canada.
Jeffrey D TurnerDefyrus , Toronto, Ontario, Canada.
Jack GauldieMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University , Hamilton, Ontario, Canada ; M.G. DeGroote Institute for Infectious Disease Research, McMaster University , Hamilton, Ontario, Canada.
Zhou XingMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University , Hamilton, Ontario, Canada ; M.G. DeGroote Institute for Infectious Disease Research, McMaster University , Hamilton, Ontario, Canada.
McMaster University Medical Centre · CAMcMaster University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pneumococcal infections are the leading cause of community-acquired pneumonia. Although the type 1 interferon-α (IFN-α) is a well-known antiviral cytokine, the role of IFN-α in antipneumococcal host defense and its therapeutic potential remain poorly understood. We have investigated these issues by using a murine transgene expression model. We found that in control animals, Streptococcus pneumoniae infection caused severe weight loss and excessive lung inflammation, associated with rapid bacterial outgrowth. In contrast, the animals that received a single dose of an adenoviral vector expressing IFN-α prior to pneumococcal infection demonstrated rapid and effective control of bacterial replication and lung inflammation and improved clinical outcome. Enhanced protection by IFN-α was due to increased activation of neutrophils and macrophages with increased release of reactive oxygen and nitrogen species and bacterial killing. Furthermore, we found that raised levels of IFN-α in the lung remained immune protective even when the gene transfer vector was given at a time postpneumococcal infection. Our study thus shows that the classically antiviral type 1 IFN can be exploited for enhancing immunity against pneumococcal infection via its activating effects on innate immune cells. Our findings hold implications for the therapeutic use of IFN-α gene transfer strategies to combat pneumococcal infections.

Indexed as

adenoviral-mediated gene transferinnate immune regulationlungpneumococcal pneumoniatype 1 interferon

Identifiers

PMID26015944
PMCPMC4378291
OpenAlexW2325834977

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.