Evidence map›Paper›PMID 20351139›Full record

ArticleInfection and immunity2010

Cooperation between multiple microbial pattern recognition systems is important for host protection against the intracellular pathogen Legionella pneumophila.

Kristina A Archer, Florence Ader, Koichi S Kobayashi, Richard A Flavell, Craig R Roy

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 54 citations in OpenAlex.

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  3. Cigarette smoke depletes alveolar macrophages and delays clearance ofAmerican journal of physiology. Lung cellular and molecular physiology · 2023
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  4. Knowledge to Predict Pathogens:Microorganisms · 2022
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  7. The Role of Nucleotide-Binding Oligomerization Domain-Like Receptors in Pulmonary Infection.American journal of respiratory cell and molecular biology · 2017
    Review
  8. Article
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  11. Article
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  16. Review
  17. 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

5 authors at 3 institutions in 2 countries.

Kristina A ArcherSection of Microbial Pathogenesis, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.
Florence Ader
Koichi S Kobayashi
Richard A Flavell
Craig R Roy
Yale University · USDana-Farber Cancer Institute · USInserm · FR

Funding

EVASION OF ANTIGEN PRESENTATION BY VACUOLAR PATHOGENSR01AI048770 · NIAID · YALE UNIVERSITY · PI ROY, CRAIG R. · 2001 to 2015
$5.8M
Nod2-mediated regulation of intestinal homeostasisR01DK074738 · NIDDK · DANA-FARBER CANCER INST · PI KOBAYASHI, KOICHI S · 2007 to 2011
$1.4M
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI048770NIAID NIH HHS R01-AI048770NIDDK NIH HHS R01 DK074738
6 · The paper itself

Abstract

Multiple pattern recognition systems have been shown to initiate innate immune responses to microbial pathogens. The degree to which these detection systems cooperate with each other to provide host protection is unknown. Here, we investigated the importance of several immune surveillance pathways in protecting mice against lethal infection by the intracellular pathogen Legionella pneumophila, the causative agent of a severe pneumonia called Legionnaires' disease. Rip2 and Naip5/NLRC4 signaling was found to contribute to the innate immune response generated against L. pneumophila in the lung. Elimination of Rip2 or Naip5/NLRC4 signaling in MyD88-deficient mice resulted in increased replication and dissemination of L. pneumophila and higher rates of mortality. Irradiated wild-type mice receiving bone marrow cells from pattern recognition receptor-deficient mice displayed L. pneumophila infection phenotypes similar to those of donor mice. Rip2 and Naip5/NLRC4 signaling provided additive effects in protecting MyD88-deficient mice from lethal infection by L. pneumophila, with the contribution of Naip5/NLRC4 being slightly greater than that of Rip2. Thus, activation of the Rip2, MyD88, and Naip5/NLRC4 signaling pathways triggers a coordinated and synergistic response that protects the host against lethal infection by L. pneumophila. These data provide new insight into how different pattern recognition systems interact functionally to generate innate immune responses that protect the host from lethal infection by activating cellular pathways that restrict intracellular replication of L. pneumophila and by recruiting to the site of infection additional phagocytes that eliminate extracellular bacteria.

Indexed as

Signal TransductionAnimalsGene Knockout TechniquesLegionella pneumophilaLegionnaires' DiseaseMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88Neuronal Apoptosis-Inhibitory ProteinReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesReceptors, ImmunologicSurvival AnalysisMyd88 protein, mouseMyeloid Differentiation Factor 88Naip5 protein, mouseNeuronal Apoptosis-Inhibitory ProteinReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesReceptors, ImmunologicRipk2 protein, mouse

Identifiers

PMID20351139
PMCPMC2876572
OpenAlexW2123945190

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.