ArticlePLoS pathogens2008
Type IV secretion-dependent activation of host MAP kinases induces an increased proinflammatory cytokine response to Legionella pneumophila.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed, 128 citations in OpenAlex.
- The conserved coordination of acyl-homoserine lactone and PqsE signaling defines the RhlR-dependent quorum-sensing network inbioRxiv : the preprint server for biology · 2026Article
- Molecular evolution and adaptations ofFrontiers in cellular and infection microbiology · 2026Review
- Article
- GM-CSF engages multiple signaling pathways to enhance pro-inflammatory cytokine responses in human monocytes duringInfection and immunity · 2025Article
- ThemSphere · 2025Article
- Different infant formulas can activate toll-like receptor 9 in vitro and inhibit interleukin 6 in human primary intestinal epithelial cells.European journal of nutrition · 2024Article
- Article
- Genetic evidence for a regulated cysteine protease catalytic triad in LegA7, abioRxiv : the preprint server for biology · 2024Article
- Role of Type 4B Secretion System Protein, IcmE, in the Pathogenesis ofPathogens (Basel, Switzerland) · 2024Article
- A Legionella toxin exhibits tRNA mimicry and glycosyl transferase activity to target the translation machinery and trigger a ribotoxic stress response.Nature cell biology · 2023Article
- Legionella pneumophila Rhizoferrin Promotes Bacterial Biofilm Formation and Growth within Amoebae and Macrophages.Infection and immunity · 2023Article
- TNF licenses macrophages to undergo rapid caspase-1, -11, and -8-mediated cell death that restricts Legionella pneumophila infection.PLoS pathogens · 2023Article
- TheProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Concept about the Virulence Factor ofMicroorganisms · 2022Review
- TNF-α response in macrophages depends on clinicalVirulence · 2022Article
- Knowledge to Predict Pathogens:Microorganisms · 2022Review
- Pathogenicity and Virulence ofVirulence · 2021Review
- Effector-triggered immunity and pathogen sensing in metazoans.Nature microbiology · 2020Review
- Legionnaires' Disease Mortality in Guinea Pigs Involves the p45 Mobile Genomic Element.The Journal of infectious diseases · 2019Article
- Viewing Legionella pneumophila Pathogenesis through an Immunological Lens.Journal of molecular biology · 2019Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The immune system must discriminate between pathogenic and nonpathogenic microbes in order to initiate an appropriate response. Toll-like receptors (TLRs) detect microbial components common to both pathogenic and nonpathogenic bacteria, whereas Nod-like receptors (NLRs) sense microbial components introduced into the host cytosol by the specialized secretion systems or pore-forming toxins of bacterial pathogens. The host signaling pathways that respond to bacterial secretion systems remain poorly understood. Infection with the pathogen Legionella pneumophila, which utilizes a type IV secretion system (T4SS), induced an increased proinflammatory cytokine response compared to avirulent bacteria in which the T4SS was inactivated. This enhanced response involved NF-kappaB activation by TLR signaling as well as Nod1 and Nod2 detection of type IV secretion. Furthermore, a TLR- and RIP2-independent pathway leading to p38 and SAPK/JNK MAPK activation was found to play an equally important role in the host response to virulent L. pneumophila. Activation of this MAPK pathway was T4SS-dependent and coordinated with TLR signaling to mount a robust proinflammatory cytokine response to virulent L. pneumophila. These findings define a previously uncharacterized host response to bacterial type IV secretion that activates MAPK signaling and demonstrate that coincident detection of multiple bacterial components enables immune discrimination between virulent and avirulent bacteria.
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.