ArticleCellular microbiology2009
Multiple MyD88-dependent responses contribute to pulmonary clearance of Legionella pneumophila.
Article in Cellular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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.
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.
Who cites it
40 citing papers in PubMed, 70 citations in OpenAlex.
- Article
- Article
- Hiding in the yolk: A unique feature of Legionella pneumophila infection of zebrafish.PLoS pathogens · 2023Article
- Cigarette smoke depletes alveolar macrophages and delays clearance ofAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
- Concept about the Virulence Factor ofMicroorganisms · 2022Review
- IRF3 inhibits IFN-γ-mediated restriction of intracellular pathogens in macrophages independently of IFNAR.Journal of leukocyte biology · 2022Article
- Pathogenicity and Virulence ofVirulence · 2021Review
- Article
- The Role of Lipids inInternational journal of molecular sciences · 2021Review
- Article
- Viewing Legionella pneumophila Pathogenesis through an Immunological Lens.Journal of molecular biology · 2019Review
- Potentiation of Cytokine-Mediated Restriction ofJournal of bacteriology · 2019Article
- Yersinia pestis Exploits Early Activation of MyD88 for Growth in the Lungs during Pneumonic Plague.Infection and immunity · 2019Article
- Neutrophils and Ly6Chi monocytes collaborate in generating an optimal cytokine response that protects against pulmonary Legionella pneumophila infection.PLoS pathogens · 2017Article
- The Type II Secretion System of Legionella pneumophila Dampens the MyD88 and Toll-Like Receptor 2 Signaling Pathway in Infected Human Macrophages.Infection and immunity · 2017Article
- Spectrum of pathogen- and model-specific histopathologies in mouse models of acute pneumonia.PloS one · 2017Article
- Cooperation between Monocyte-Derived Cells and Lymphoid Cells in the Acute Response to a Bacterial Lung Pathogen.PLoS pathogens · 2016Article
- The Sphingosine-1-Phosphate Lyase (LegS2) Contributes to the Restriction of Legionella pneumophila in Murine Macrophages.PloS one · 2016Article
- A new way to detect the danger: Lysosomal cell death induced by a bacterial ribosomal protein.Journal of nature and science · 2015Article
- Subversion of Cell-Autonomous Immunity and Cell Migration by Legionella pneumophila Effectors.Frontiers in immunology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
MyD88-dependent signalling is important for secretion of early inflammatory cytokines and host protection in response to Legionella pneumophila infection. Although toll-like receptor (TLR)2 contributes to MyD88-dependent clearance of L. pneumophila, TLR-independent functions of MyD88 could also be important. To determine why MyD88 is critical for host protection to L. pneumophila, the contribution of multiple TLRs and IL-18 receptor (IL-18R)-dependent interferon-gamma (IFN-gamma) production in a mouse was examined. Mice deficient for TLR5 or TLR9, or deficient for TLR2 along with either TLR5 or TLR9, were competent for controlling bacterial replication and had no apparent defects in cytokine production compared with control mice. MyD88-dependent production of IFN-gamma in the lung was mediated primarily by natural killer cells and required IL-18R signalling. Reducing IFN-gamma levels did not greatly affect the kinetics of L. pneumophila replication or clearance in infected mice. Additionally, IFN-gamma-deficient mice did not have a susceptibility phenotype as severe as the MyD88-deficient mice and were able to control a pulmonary infection by L. pneumophila. Thus, MyD88-dependent innate immune responses induced by L. pneumophila involve both TLR-dependent responses and IL-18R-dependent production of IFN-gamma by natural killer cells, and these MyD88-dependent pathways can function independently to provide host protection against an intracellular pathogen.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.