Evidence map›Paper›PMID 19805527›Full record

ArticleInfection and immunity2009

Inescapable need for neutrophils as mediators of cellular innate immunity to acute Pseudomonas aeruginosa pneumonia.

Andrew Y Koh, Gregory P Priebe, Christopher Ray, Nico Van Rooijen, Gerald B Pier

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

138 citing papers in PubMed, 181 citations in OpenAlex.

  1. Trial
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78 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 4 institutions in 2 countries.

Andrew Y KohChanning Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Andrew.Koh@UTSouthwestern.edu
Gregory P Priebe
Christopher Ray
Nico Van Rooijen
Gerald B Pier
Brigham and Women's Hospital · USDana-Farber Cancer Institute · USOffice of Infectious Diseases · USUniversity of Amsterdam · NL

Funding

POLYSACCHARIDE VACCINE FOR PSEUDOMONAS AERUGINOSAR01AI022535 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI PIER, GERALD B · 1985 to 2009
$3.4M
VIRULENCE AND IMMUNITY TO MUCOID P. AERUGINOSAR01AI048917 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI PIER, GERALD B · 2001 to 2009
$3.2M
Cellular immunity to P. aeruginosa candidate vaccinesK08AI050036 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI PRIEBE, GREGORY P · 2001 to 2005
$621k
Mucosal colonization and dissemination of P. aeruginosaK08AI062983 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI KOH, ANDREW · 2005 to 2009
$619k
NIAID NIH HHS AI48917NIAID NIH HHS AI 50036NIAID NIH HHS AI62983NIAID NIH HHS K08 AI050036NIAID NIH HHS K08 AI062983NIAID NIH HHS N01 AI050036NIAID NIH HHS R01 AI022535NIAID NIH HHS R01 AI048917NIAID NIH HHS R01 AI22535
6 · The paper itself

Abstract

Pseudomonas aeruginosa is a leading cause of pneumonia, and many components of the innate immune system have been proposed to exert important effects in preventing lung infection. However, a vigorous experimental system to identify an overriding, key effector mediating innate immunity to lung infection has not been utilized. As many of the important components of innate immunity are involved in recruitment and activation of polymorphonuclear neutrophils (PMNs) to infected tissues, we hypothesized that the cells and factors needed for their proper recruitment to the lung comprised the major mediators of innate immunity. In neutropenic mice, intranasal (i.n.) doses of P. aeruginosa as low as 10 to 100 CFU/mouse produced a fatal lung infection, compared with 10(7) to >10(8) CFU for nonneutropenic mice. There was only a very modest increased mortality in mice lacking mature lymphocytes and no increased mortality in mice depleted of alveolar macrophages when administered i.n. P. aeruginosa. Recombinant mouse granulocyte colony-stimulating factor increased survival of neutropenic mice after i.n. P. aeruginosa inoculation. MyD88(-/-) mice, which cannot recruit PMNs to the lungs, were highly susceptible to fatal P. aeruginosa lung infection, with bacterial doses of <120 CFU being lethal. Activation of a MyD88-independent pathway for PMN recruitment to the lungs in MyD88(-/-) mice resulted in enhanced protection against P. aeruginosa lung infection. Overall, in the absence of PMNs, mice cannot resist P. aeruginosa lung infection from extremely small bacterial doses. There is an inescapable requirement for local PMN recruitment and activation to mediate innate immunity to P. aeruginosa lung infection.

Indexed as

Immunity, InnateAnimalsDisease SusceptibilityFemaleLungLymphocytesMacrophages, AlveolarMiceMice, Inbred C3HMice, Inbred C57BLMice, KnockoutNeutrophilsPneumonia, BacterialPseudomonas aeruginosaPseudomonas InfectionsSurvival Analysis

Identifiers

PMID19805527
PMCPMC2786465
OpenAlexW2169899985

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.