Evidence map›Paper›PMID 21321074›Full record

ArticleInfection and immunity2011

Analysis of murine genetic predisposition to pneumococcal infection reveals a critical role of alveolar macrophages in maintaining the sterility of the lower respiratory tract.

Keer Sun, Yan Gan, Dennis W Metzger

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
  6. Hydrogen sulfide dysregulates the immune response by suppressing central carbon metabolism to promote tuberculosis.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  7. Article
  8. Genetic Models of Macrophage Depletion.Methods in molecular biology (Clifton, N.J.) · 2018
    Review
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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.

Keer SunCenter for Immunology and Microbial Disease, MC-151, Albany Medical College, 47 New Scotland Avenue, Albany, NY 12208, USA. Sunk@mail.amc.edu
Yan Gan
Dennis W Metzger
Albany Medical Center Hospital · US

Funding

Identification of genes that affect peak BMD in men and womenR01AG041517 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI ECONS, MICHAEL J · 2011 to 2015
$2.9M
Effect of Influenza Infection on Alveolar Macrophage FunctionR01AI075312 · NIAID · ALBANY MEDICAL COLLEGE · PI METZGER, DENNIS W · 2009 to 2012
$1.6M
NIAID NIH HHS R01 AI075312NIAID NIH HHS R01 AI41517NIAID NIH HHS R01 AI75312NIA NIH HHS R01 AG041517
6 · The paper itself

Abstract

The study of pathogenic mechanisms of disease can be greatly facilitated by studying genetic differences in susceptibility to infection. In the present study, we compared the severity of pneumococcal infection in C57BL/6 (B6) and 129Sv mice. The results showed that 129Sv mice were remarkably more susceptible to pneumococcal infection than B6 mice. Bacterial clearance, proinflammatory mediators, leukocyte recruitment, and phagocyte activities were measured to examine potential immune factors associated with differences in susceptibility to pneumococcal infection. The greater susceptibility of 129Sv mice was associated only with inadequate alveolar macrophage bacterial killing, as indicated by significantly decreased initial bacterial clearance from the respiratory tract. Effective pneumococcal clearance was not dependent upon Toll-like receptor 2 (TLR2) expression, oxidative stress, or matrix metallopeptidase 12 (MMP-12) expression. Furthermore, phagocytosis analysis suggested that the deficiency found in 129Sv alveolar macrophages was not due to a lack of bacterial recognition but, rather, to reduced bacterial uptake. In conclusion, our findings indicate a crucial role of alveolar macrophage phagocytosis during innate defense against pneumococcal infection, which may explain the association of host genetic risk factors with predisposition to pneumococcal infection.

Indexed as

AnimalsCell SeparationEnzyme-Linked Immunosorbent AssayFlow CytometryFluorescent Antibody TechniqueGenetic Predisposition to DiseaseLungMacrophages, AlveolarMiceMice, 129 StrainMice, Inbred C57BLMicroscopy, ConfocalPneumonia, Pneumococcal

Identifiers

PMID21321074
PMCPMC3088159
OpenAlexW2106549921

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.