Evidence map›Paper›PMID 25058342›Full record

ArticlePLoS pathogens2014

The frustrated host response to Legionella pneumophila is bypassed by MyD88-dependent translation of pro-inflammatory cytokines.

Seblewongel Asrat, Aisling S Dugan, Ralph R Isberg

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 65 citations in OpenAlex.

  1. Molecular evolution and adaptations ofFrontiers in cellular and infection microbiology · 2026
    Review
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  4. ThemSphere · 2025
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  5. Journal of bacteriology · 2024
    Review
  6. iScience · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Microorganisms · 2022
    Article
  11. Glycosylating Effectors ofBiomolecules · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Mechanisms of Effector-Mediated Immunity Revealed by the Accidental Human PathogenFrontiers in cellular and infection microbiology · 2020
    Review
  20. Review
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

3 authors at 2 institutions in 1 country.

Seblewongel AsratHoward Hughes Medical Institute, Boston, Massachusetts, United States of America; Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America; Graduate Program in Molecular Microbiology, Sackler School of Graduate Biomedical Science, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Aisling S DuganDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Ralph R IsbergHoward Hughes Medical Institute, Boston, Massachusetts, United States of America; Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Tufts University · USHoward Hughes Medical Institute · US

Funding

Training in Education and Critical Research SkillsK12GM074869 · NIGMS · TUFTS UNIVERSITY BOSTON · PI MOORE, CLAIRE L · 2006 to 2017
$8.5M
Dissecting the Role of ERK and DUSP of Legionella pneumophila InfectionF32AI084202 · NIAID · TUFTS UNIVERSITY BOSTON · PI DUGAN, AISLING SIOBHAN · 2009 to 2009
$41k
Howard Hughes Medical InstituteNIAID NIH HHS F32 AI084202NIAID NIH HHS F32AI084202NIGMS NIH HHS 5K12GM074869NIGMS NIH HHS K12 GM074869
6 · The paper itself

Abstract

Many pathogens, particularly those that require their host for survival, have devised mechanisms to subvert the host immune response in order to survive and replicate intracellularly. Legionella pneumophila, the causative agent of Legionnaires' disease, promotes intracellular growth by translocating proteins into its host cytosol through its type IV protein secretion machinery. At least 5 of the bacterial translocated effectors interfere with the function of host cell elongation factors, blocking translation and causing the induction of a unique host cell transcriptional profile. In addition, L. pneumophila also interferes with translation initiation, by preventing cap-dependent translation in host cells. We demonstrate here that protein translation inhibition by L. pneumophila leads to a frustrated host MAP kinase response, where genes involved in the pathway are transcribed but fail to be translated due to the bacterium-induced protein synthesis inhibition. Surprisingly, few pro-inflammatory cytokines, such as IL-1α and IL-1β, bypass this inhibition and get synthesized in the presence of Legionella effectors. We show that the selective synthesis of these genes requires MyD88 signaling and takes place in both infected cells that harbor bacteria and neighboring bystander cells. Our findings offer a perspective of how host cells are able to cope with pathogen-encoded activities that disrupt normal cellular process and initiate a successful inflammatory response.

Indexed as

AnimalsHumansInterleukin-1alphaInterleukin-1betaLegionella pneumophilaLegionnaires' DiseaseMiceMice, KnockoutMyeloid Differentiation Factor 88Protein BiosynthesisU937 CellsIL1A protein, humanIL1B protein, humanIL1B protein, mouseInterleukin-1alphaInterleukin-1betaMYD88 protein, humanMyd88 protein, mouseMyeloid Differentiation Factor 88

Identifiers

PMID25058342
PMCPMC4110041
OpenAlexW1968777463

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.