Evidence map›Paper›PMID 24244159›Full record

ArticlePLoS pathogens2013

Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.

Kim S LeMessurier, Hans Häcker, Liying Chi, Elaine Tuomanen, Vanessa Redecke

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

74 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
  2. Myeloid cell reprogramming drives enhanced defense againstProceedings of the National Academy of Sciences of the United States of America · 2026
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  20. ImmunobioticInternational journal of molecular sciences · 2023
    Article

14 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

5 authors at 1 institution in 1 country.

Kim S LeMessurierDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
Hans Häcker
Liying Chi
Elaine Tuomanen
Vanessa Redecke
St. Jude Children's Research Hospital · US

Funding

PNEUMOCOCCAL CELL WALL IN MENINGITISR01AI027913 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI TUOMANEN, ELAINE I · 1989 to 2015
$5.2M
TLR-mediated Signaling Complex Formation and Regulation of Effector FunctionsR01AI083443 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI HAECKER, HANS · 2009 to 2012
$1.7M
NIAID NIH HHS AI083443NIAID NIH HHS AI27913NIAID NIH HHS R01 AI027913NIAID NIH HHS R01 AI083443
6 · The paper itself

Abstract

Streptococcus pneumoniae infection is a leading cause of bacterial pneumonia, sepsis and meningitis and is associated with high morbidity and mortality. Type I interferon (IFN-I), whose contribution to antiviral and intracellular bacterial immunity is well established, is also elicited during pneumococcal infection, yet its functional significance is not well defined. Here, we show that IFN-I plays an important role in the host defense against pneumococci by counteracting the transmigration of bacteria from the lung to the blood. Mice that lack the type I interferon receptor (Ifnar1 (-/-)) or mice that were treated with a neutralizing antibody against the type I interferon receptor, exhibited enhanced development of bacteremia following intranasal pneumococcal infection, while maintaining comparable bacterial numbers in the lung. In turn, treatment of mice with IFNβ or IFN-I-inducing synthetic double stranded RNA (poly(I:C)), dramatically reduced the development of bacteremia following intranasal infection with S. pneumoniae. IFNβ treatment led to upregulation of tight junction proteins and downregulation of the pneumococcal uptake receptor, platelet activating factor receptor (PAF receptor). In accordance with these findings, IFN-I reduced pneumococcal cell invasion and transmigration across epithelial and endothelial layers, and Ifnar1 (-/-) mice showed overall enhanced lung permeability. As such, our data identify IFN-I as an important component of the host immune defense that regulates two possible mechanisms involved in pneumococcal invasion, i.e. PAF receptor-mediated transcytosis and tight junction-dependent pericellular migration, ultimately limiting progression from a site-restricted lung infection to invasive, lethal disease.

Indexed as

AnimalsBacteremiaBlood-Air BarrierBlood-Brain BarrierInterferon Type IMiceMice, KnockoutPneumonia, PneumococcalReceptor, Interferon alpha-betaStreptococcus pneumoniaeIfnar1 protein, mouseInterferon Type IReceptor, Interferon alpha-beta

Identifiers

PMID24244159
PMCPMC3820719
OpenAlexW2040555386

What OpenQuestion holds

Textmetadata
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.