Evidence map›Paper›PMID 25876764›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Integrated innate mechanisms involved in airway allergic inflammation to the serine protease subtilisin.

Esther Florsheim, Shuang Yu, Ivan Bragatto, Lucas Faustino, Eliane Gomes, Rodrigo N Ramos, José Alexandre M Barbuto, Ruslan Medzhitov, Momtchilo Russo

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Immune sensing of food allergens promotes aversive behaviour.bioRxiv : the preprint server for biology · 2023
    Article
  6. Article
  7. Article
  8. Journal of fungi (Basel, Switzerland) · 2020
    Review
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  12. Article
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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

9 authors at 2 institutions in 3 countries.

Esther FlorsheimDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, 05508-000 SP Brazil; Department of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510; and.ORCID http://orcid.org/0000-0002-5889-7442
Shuang YuDepartment of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510; and.
Ivan BragattoDepartment of Biochemistry, Institute of Chemistry, University of Sao Paulo, Sao Paulo, 05508-000 SP Brazil.
Lucas FaustinoDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, 05508-000 SP Brazil;
Eliane GomesDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, 05508-000 SP Brazil;
Rodrigo N RamosDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, 05508-000 SP Brazil;
José Alexandre M BarbutoDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, 05508-000 SP Brazil;
Ruslan MedzhitovDepartment of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510; and.
Momtchilo RussoDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, 05508-000 SP Brazil; momrusso@icb.usp.br.
Universidade de São Paulo · BRHoward Hughes Medical Institute · US

Funding

Cell Biology of TLR Signal TransductionR37AI046688 · NIAID · YALE UNIVERSITY · PI MEDZHITOV, RUSLAN · 2006 to 2015
$3.8M
TLRs in Host Commensal InteractionsR01DK071754 · NIDDK · YALE UNIVERSITY · PI MEDZHITOV, RUSLAN · 2007 to 2014
$2.8M
Role of basophils in initiating Th2 immune responsesR01AI089771 · NIAID · YALE UNIVERSITY · PI MEDZHITOV, RUSLAN · 2010 to 2014
$2.0M
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI089771NIAID NIH HHS R37 AI046688NIDDK NIH HHS R01 DK071754
6 · The paper itself

Abstract

Proteases are recognized environmental allergens, but little is known about the mechanisms responsible for sensing enzyme activity and initiating the development of allergic inflammation. Because usage of the serine protease subtilisin in the detergent industry resulted in an outbreak of occupational asthma in workers, we sought to develop an experimental model of allergic lung inflammation to subtilisin and to determine the immunological mechanisms involved in type 2 responses. By using a mouse model of allergic airway disease, we have defined in this study that s.c. or intranasal sensitization followed by airway challenge to subtilisin induces prototypic allergic lung inflammation, characterized by airway eosinophilia, type 2 cytokine release, mucus production, high levels of serum IgE, and airway reactivity. These allergic responses were dependent on subtilisin protease activity, protease-activated receptor-2, IL-33R ST2, and MyD88 signaling. Also, subtilisin stimulated the expression of the proallergic cytokines IL-1α, IL-33, thymic stromal lymphopoietin, and the growth factor amphiregulin in a human bronchial epithelial cell line. Notably, acute administration of subtilisin into the airways increased lung IL-5-producing type 2 innate lymphoid cells, which required protease-activated receptor-2 expression. Finally, subtilisin activity acted as a Th2 adjuvant to an unrelated airborne Ag-promoting allergic inflammation to inhaled OVA. Therefore, we established a murine model of occupational asthma to a serine protease and characterized the main molecular pathways involved in allergic sensitization to subtilisin that potentially contribute to initiate allergic airway disease.

Indexed as

Disease Models, AnimalAdultAllergensAnimalsAsthma, OccupationalCell LineDendritic CellsFemaleFlow CytometryHumansImmunity, InnateInflammationMiceMice, Inbred C57BLMice, KnockoutSubtilisinAllergensSubtilisin

Identifiers

PMID25876764
PMCPMC4417417
OpenAlexW1943034182

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.