Evidence map›Paper›PMID 21572023›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Airway epithelial MyD88 restores control of Pseudomonas aeruginosa murine infection via an IL-1-dependent pathway.

Lilia A Mijares, Tamding Wangdi, Caroline Sokol, Robert Homer, Ruslan Medzhitov, Barbara I Kazmierczak

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

54 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Flagellum-deficientMicrobiology spectrum · 2024
    Article
  4. Article
  5. Frontiers in immunology · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Monoclonal antibodies against lipopolysaccharide protect againstFrontiers in cellular and infection microbiology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. UnderstandingCells · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Integrative Physiology of Pneumonia.Physiological reviews · 2018
    Review
  20. The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Article
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

6 authors at 2 institutions in 1 country.

Lilia A MijaresYale University School of Medicine, New Haven, CT 06520, USA.
Tamding Wangdi
Caroline Sokol
Robert Homer
Ruslan Medzhitov
Barbara I Kazmierczak
Yale University · USVA Connecticut Healthcare System · US

Funding

Innate Immune Responses to Type 3 Secretion System Components and EffectorsR01AI081825 · NIAID · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 2010 to 2013
$1.7M
Innate Response Events in Respiratory Epithelial CellsF31AI061882 · NIAID · YALE UNIVERSITY · PI MIJARES, LILIA A. · 2004 to 2007
$135k
Howard Hughes Medical InstituteNIAID NIH HHS F31 AI061882NIAID NIH HHS R01 AI081825
6 · The paper itself

Abstract

The opportunistic human pathogen Pseudomonas aeruginosa causes rapidly progressive and tissue-destructive infections, such as hospital-acquired and ventilator-associated pneumonias. Innate immune responses are critical in controlling P. aeruginosa in the mammalian lung, as demonstrated by the increased susceptibility of MyD88(-/-) mice to this pathogen. Experiments conducted using bone marrow chimeric mice demonstrated that radio-resistant cells participated in initiating MyD88-dependent innate immune responses to P. aeruginosa. In this study we used a novel transgenic mouse model to demonstrate that MyD88 expression by epithelial cells is sufficient to generate a rapid and protective innate immune response following intranasal infection with P. aeruginosa. MyD88 functions as an adaptor for many TLRs. However, mice in which multiple TLR pathways (e.g., TLR2/TLR4/TLR5) are blocked are not as compromised in their response to P. aeruginosa as mice lacking MyD88. We demonstrate that IL-1R signaling is an essential element of MyD88-dependent epithelial cell responses to P. aeruginosa infection.

Indexed as

AnimalsHumansImmunity, InnateInterleukin-1MiceMice, KnockoutMyeloid Differentiation Factor 88Pseudomonas aeruginosaPseudomonas InfectionsRespiratory MucosaSignal TransductionInterleukin-1Myd88 protein, mouseMyeloid Differentiation Factor 88

Identifiers

PMID21572023
PMCPMC3110630
OpenAlexW2100755491

What OpenQuestion holds

Textmetadata
LicenceTDM
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.