Evidence map›Paper›PMID 21864623›Full record

ArticleVaccine2011

The innate immune response to Streptococcus pneumoniae in the lung depends on serotype and host response.

Beza Seyoum, Masahide Yano, Liise-anne Pirofski

Abstract readComparative Study
In one paragraph

Article in Vaccine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
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  6. Article
  7. Absence ofMicroorganisms · 2022
    Article
  8. Contribution of Puma to Inflammatory Resolution During Early Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022
    Article
  9. Neutrophil Recruitment in Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
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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

3 authors at 1 institution in 1 country.

Beza SeyoumDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Masahide Yano
Liise-anne Pirofski
Albert Einstein College of Medicine · US

Funding

VARIABLE GENE USE AND PNEUMOCOCCAL IMMUNITY IN AIDSR01AI045459 · NIAID · YESHIVA UNIVERSITY · PI PIROFSKI, LIISE-ANNE · 2000 to 2010
$3.9M
VARIABLE GENE DEFECTS AND PNEUMOCOCCAL SUSCEPTIBILITYR01AI044374 · NIAID · YESHIVA UNIVERSITY · PI PIROFSKI, LIISE-ANNE · 2001 to 2010
$2.7M
NIAID NIH HHS R01 AI044374NIAID NIH HHS R01-AI044374NIAID NIH HHS R01 AI045459NIAID NIH HHS R01-AI045459PHS HHS T32-A107506
6 · The paper itself

Abstract

Bacteremic pneumonia with some pneumococcal capsular serotypes, including serotype 3 (ST3), has been associated with a higher risk of death, whereas others, such as ST8, are associated with a lower risk. To provide a molecular basis for understanding such differences, we used oligo cDNA microarrays to analyze and compare the gene expression profiles of the lungs of Balb/c mice infected intranasally with either ST3, strain A66.1, or ST8, strain ATCC 6308 (6308). Compared to uninfected controls, infection with either A66.1 or 6308 led to inoculum-dependent expression of IFN-γ inducible CXC chemokines among other pro-inflammatory genes. To investigate the role that IFN-γ inducible chemokines CXCL9, CXCL10 and CXCL11 play in A66.1- and 6308-induced pneumonia, we examined the effect of the absence of their common receptor, CXCR3, on intranasal infection in CXCR3(-/-) (Balb/c) mice. Compared to wild type (WT) mice, virulence of A66.1 but not 6308 was attenuated in CXCR3(-/-) mice. A66.1-infected CXCR3(-/-) mice had fewer lung neutrophils and more alveolar macrophages 48 h after infection and fewer blood CFU 72 h after infection. Histopathological examination of lung sections revealed less inflammation among A66.1-infected CXCR3(-/-) than WT mice. The reduced virulence of A66.1 in CXCR3(-/-) mice suggests that inhibition of the functional activity of IFN-γ inducible chemokines modulates the host response to A66.1, in turn suggesting a novel approach to improve vaccine-mediated protection against ST3 pneumonia.

Indexed as

Host-Pathogen InteractionsImmunity, InnateAnimalsChemokinesFemaleGene Expression ProfilingHumansLungMacrophages, AlveolarMiceMice, Inbred BALB CMice, KnockoutNeutrophilsStreptococcus pneumoniaeTime FactorsChemokines

Identifiers

PMID21864623
PMCPMC3191269
OpenAlexW2069114357

What OpenQuestion holds

Textmetadata
LicenceTDM
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.