Evidence map›Paper›PMID 19864598›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Recognition of fungal protease activities induces cellular activation and eosinophil-derived neurotoxin release in human eosinophils.

Yoshinori Matsuwaki, Kota Wada, Thomas A White, Linda M Benson, M Cristine Charlesworth, James L Checkel, Yoshinari Inoue, Kyoko Hotta, Jens U Ponikau, Christopher B Lawrence and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. First Reported Case of a Clinically Nonresponsive-to-ItraconazoleJournal of fungi (Basel, Switzerland) · 2023
    Article
  5. Review
  6. Immunopathologic Role of Eosinophils in Eosinophilic Chronic Rhinosinusitis.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Revisiting the controversy: The role of fungi in chronic rhinosinusitis.International forum of allergy & rhinology · 2021
    Review
  9. Review
  10. Mechanisms of eosinophilic inflammation.Asia Pacific allergy · 2020
    Review
  11. Review
  12. Innate and adaptive immune responses to fungi in the airway.The Journal of allergy and clinical immunology · 2018
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. A Player and Coordinator: The Versatile Roles of Eosinophils in the Immune System.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2016
    Review
  19. Airway surface mycosis in chronic TH2-associated airway disease.The Journal of allergy and clinical immunology · 2014
    Article
  20. 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

11 authors at 5 institutions in 2 countries.

Yoshinori MatsuwakiDepartment of Medicine and Immunology, Mayo Clinic, Rochester, MN 55905, USA.
Kota Wada
Thomas A White
Linda M Benson
M Cristine Charlesworth
James L Checkel
Yoshinari Inoue
Kyoko Hotta
Jens U Ponikau
Christopher B Lawrence
Hirohito Kita
Mayo Clinic · USMayo Clinic in Arizona · USMayo Clinic in Florida · USUniversity at Buffalo, State University of New York · USVirginia Tech · US

Funding

The Pathogenesis of Chronic RhinosinusitisR01AI049235 · NIAID · MAYO CLINIC ROCHESTER · PI KITA, HIROHITO · 2001 to 2011
$4.5M
MECHANISMS OF EOSINOPHIL DEGRANULATION IN HUMAN DISEASER01AI034486 · NIAID · MAYO CLINIC ROCHESTER · PI KITA, HIROHITO · 2000 to 2010
$3.2M
Mechanisms of Eosinophilic Inflammation in Human DiseaseR56AI034486 · NIAID · MAYO CLINIC ROCHESTER · PI KITA, HIROHITO · 2005 to 2012
$769k
The Pathogenesis of Chronic RhinosinusitisR56AI049235 · NIAID · MAYO CLINIC ROCHESTER · PI KITA, HIROHITO · 2012 to 2012
$278k
MECHANISMS OF EOSINOPHIL DEGRANULATIONR29AI034486 · NIAID · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI KITA, HIROHITO · 1994 to 1998
–
NIAID NIH HHS AI34486NIAID NIH HHS AI49235NIAID NIH HHS R01 AI034486NIAID NIH HHS R01 AI049235NIAID NIH HHS R29 AI034486NIAID NIH HHS R56 AI034486NIAID NIH HHS R56 AI049235
6 · The paper itself

Abstract

Eosinophils are multifunctional leukocytes implicated in the pathogenesis of asthma and in immunity to certain organisms. Associations between exposure to an environmental fungus, such as Alternaria, and asthma have been recognized clinically. Protease-activated receptors (PARs) are G protein-coupled receptors that are cleaved and activated by serine proteases, but their roles in innate immunity remain unknown. We previously found that human eosinophils respond vigorously to Alternaria organisms and to the secretory product(s) of Alternaria with eosinophils releasing their proinflammatory mediators. In this study, we investigated the roles of protease(s) produced by Alternaria and of PARs expressed on eosinophils in their immune responses against fungal organisms. We found that Alternaria alternata produces aspartate protease(s) and that human peripheral blood eosinophils degranulate in response to the cell-free extract of A. alternata. Eosinophils showed an increased intracellular calcium concentration in response to Alternaria that was desensitized by peptide and protease ligands for PAR-2 and inhibited by a PAR-2 antagonistic peptide. Alternaria-derived aspartate protease(s) cleaved PAR-2 to expose neo-ligands; these neo-ligands activated eosinophil degranulation in the absence of proteases. Finally, treatment of Alternaria extract with aspartate protease inhibitors, which are conventionally used for HIV-1 and other microbes, attenuated the eosinophils' responses to Alternaria. Thus, fungal aspartate protease and eosinophil PAR-2 appear critical for the eosinophils' innate immune response to certain fungi, suggesting a novel mechanism for pathologic inflammation in asthma and for host-pathogen interaction.

Indexed as

AlternariaAspartic Acid ProteasesAsthmaCalciumCell DegranulationEosinophil-Derived NeurotoxinEosinophilsFungal ProteinsHumansImmunity, InnatePeptidesReceptor, PAR-2Serine ProteasesAspartic Acid ProteasesCalciumEosinophil-Derived NeurotoxinFungal ProteinsPeptidesReceptor, PAR-2Serine Proteases

Identifiers

PMID19864598
PMCPMC2843542
OpenAlexW2104831363

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.