ArticleInfection and immunity2014
Alveolar macrophages and neutrophils are the primary reservoirs for Legionella pneumophila and mediate cytosolic surveillance of type IV secretion.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 76 citations in OpenAlex.
- Diverse infection models demonstrate robust resistance ofbioRxiv : the preprint server for biology · 2026Article
- Patatin-domain-containing (phospho)lipases under control: Mammalian co-regulators and pathogenic activation mechanisms.FEBS open bio · 2026Review
- Molecular evolution and adaptations ofFrontiers in cellular and infection microbiology · 2026Review
- CXCL1 augments host defense against Legionella pneumophila through the IL-18-IFN-γ axis and neutrophil homeostasis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
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- IL-1beta expressing neutrophil extracellular traps inFrontiers in immunology · 2025Article
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- Hiding in the yolk: A unique feature of Legionella pneumophila infection of zebrafish.PLoS pathogens · 2023Article
- Interaction between alveolar macrophages and epithelial cells duringFrontiers in cellular and infection microbiology · 2023Review
- Recruitment of heterologous substrates by bacterial secretion systems for transkingdom translocation.Frontiers in cellular and infection microbiology · 2023Review
- Concept about the Virulence Factor ofMicroorganisms · 2022Review
- AtypicalScience advances · 2022Article
- Screening for eukaryotic motifs inVirulence · 2022Article
- Cbp1, a fungal virulence factor under positive selection, forms an effector complex that drives macrophage lysis.PLoS pathogens · 2022Article
- Overview of the Clinical and Molecular Features of Legionella Pneumophila: Focus on Novel Surveillance and Diagnostic Strategies.Antibiotics (Basel, Switzerland) · 2022Review
- Breathe In, Breathe Out: Metabolic Regulation of Lung Macrophages in Host Defense Against Bacterial Infection.Frontiers in cellular and infection microbiology · 2022Review
- Using Genomic Deletion Mutants to Investigate Effector-Triggered Immunity During Legionella pneumophila Infection.Methods in molecular biology (Clifton, N.J.) · 2022Article
- SdhA blocks disruption of the Legionella-containing vacuole by hijacking the OCRL phosphatase.Cell reports · 2021Article
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Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Legionella pneumophila, an intracellular pathogen responsible for the severe pneumonia Legionnaires' disease, uses its dot/icm-encoded type IV secretion system (T4SS) to translocate effector proteins that promote its survival and replication into the host cell cytosol. However, by introducing bacterial products into the host cytosol, L. pneumophila also activates cytosolic immunosurveillance pathways, thereby triggering robust proinflammatory responses that mediate the control of infection. Thus, the pulmonary cell types that L. pneumophila infects not only may act as an intracellular niche that facilitates its pathogenesis but also may contribute to the immune response against L. pneumophila. The identity of these host cells remains poorly understood. Here, we developed a strain of L. pneumophila producing a fusion protein consisting of β-lactamase fused to the T4SS-translocated effector RalF, which allowed us to track cells injected by the T4SS. Our data reveal that alveolar macrophages and neutrophils both are the primary recipients of T4SS-translocated effectors and harbor viable L. pneumophila during pulmonary infection of mice. Moreover, both alveolar macrophages and neutrophils from infected mice produced tumor necrosis factor and interleukin-1α in response to T4SS-sufficient, but not T4SS-deficient, L. pneumophila. Collectively, our data suggest that alveolar macrophages and neutrophils are both an intracellular reservoir for L. pneumophila and a source of proinflammatory cytokines that contribute to the host immune response against L. pneumophila during pulmonary infection.
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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.