Mast cells contribute to the resolution of allergic inflammation by releasing resolvin D1.


Journal

Pharmacological research
ISSN: 1096-1186
Titre abrégé: Pharmacol Res
Pays: Netherlands
ID NLM: 8907422

Informations de publication

Date de publication:
03 2023
Historique:
received: 13 01 2023
revised: 03 02 2023
accepted: 06 02 2023
pmc-release: 01 03 2024
pubmed: 12 2 2023
medline: 15 3 2023
entrez: 11 2 2023
Statut: ppublish

Résumé

Mast cells are initiators and main effectors of allergic inflammation, together with eosinophils, with whom they can interact in a physical and soluble cross-talk with marked pro-inflammatory features, the Allergic Effector Unit. The pro-resolution role of mast cells, alone or in co-culture with eosinophils, has not been characterized yet. We aimed to investigate select pro-resolution pathways in mast cells in vitro and in vivo in allergic inflammation. In vitro, we employed human and murine mast cells and analyzed release of resolvin D1 and expression of 15-lipoxygenase after IgE-mediated activation. We performed co-culture of IgE-activated mast cells with peripheral blood eosinophils and investigated 15-lipoxygenase expression and Resolvin D1 release. In vivo, we performed Ovalbumin/Alum and Ovalbumin/S. aureus enterotoxin B allergic peritonitis model in Wild Type mice following a MC "overshoot" protocol. We found that IgE-activated mast cells release significant amounts of resolvin D1 30 min after activation, while 15-lipoxygenase expression remained unchanged. Resolvin D1 release was found to be decreased in IgE-activated mast cells co-cultured with peripheral blood eosinophils for 30 min In vivo, mast cell-overshoot mice exhibited a trend of reduced inflammation, together with increased peritoneal resolvin D1 release. Mast cells can actively contribute to resolution of allergic inflammation by releasing resolvin D1.

Sections du résumé

BACKGROUND
Mast cells are initiators and main effectors of allergic inflammation, together with eosinophils, with whom they can interact in a physical and soluble cross-talk with marked pro-inflammatory features, the Allergic Effector Unit. The pro-resolution role of mast cells, alone or in co-culture with eosinophils, has not been characterized yet.
OBJECTIVES
We aimed to investigate select pro-resolution pathways in mast cells in vitro and in vivo in allergic inflammation.
METHODS
In vitro, we employed human and murine mast cells and analyzed release of resolvin D1 and expression of 15-lipoxygenase after IgE-mediated activation. We performed co-culture of IgE-activated mast cells with peripheral blood eosinophils and investigated 15-lipoxygenase expression and Resolvin D1 release. In vivo, we performed Ovalbumin/Alum and Ovalbumin/S. aureus enterotoxin B allergic peritonitis model in Wild Type mice following a MC "overshoot" protocol.
RESULTS
We found that IgE-activated mast cells release significant amounts of resolvin D1 30 min after activation, while 15-lipoxygenase expression remained unchanged. Resolvin D1 release was found to be decreased in IgE-activated mast cells co-cultured with peripheral blood eosinophils for 30 min In vivo, mast cell-overshoot mice exhibited a trend of reduced inflammation, together with increased peritoneal resolvin D1 release.
CONCLUSIONS
Mast cells can actively contribute to resolution of allergic inflammation by releasing resolvin D1.

Identifiants

pubmed: 36773709
pii: S1043-6618(23)00047-6
doi: 10.1016/j.phrs.2023.106691
pmc: PMC10285510
mid: NIHMS1875331
pii:
doi:

Substances chimiques

Ovalbumin 9006-59-1
resolvin D1 0
Arachidonate 15-Lipoxygenase EC 1.13.11.33
Immunoglobulin E 37341-29-0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

106691

Subventions

Organisme : NIGMS NIH HHS
ID : P01 GM095467
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL122531
Pays : United States

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interests statement The authors have declared that no conflict of interest exists.

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Auteurs

Pier Giorgio Puzzovio (PG)

Pharmacology and Experimental Therapeutics Unit, School of Pharmacy, Institute for Drug Research, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.

Hadas Pahima (H)

Pharmacology and Experimental Therapeutics Unit, School of Pharmacy, Institute for Drug Research, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.

Tresa George (T)

Pharmacology and Experimental Therapeutics Unit, School of Pharmacy, Institute for Drug Research, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.

David Mankuta (D)

Department of Obstetrics and Gynecology, Hadassah Hebrew University Medical Center, Jerusalem, Israel.

Ron Eliashar (R)

Department of Otolaryngology / Head and Neck Surgery, Hadassah Hebrew University Medical Center and the Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.

Ekaterini Tiligada (E)

Pharmacology and Experimental Therapeutics Unit, School of Pharmacy, Institute for Drug Research, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel; Department of Pharmacology, Medical School, National and Kapodistrian University of Athens, Athens, Greece.

Bruce D Levy (BD)

Pulmonary and Critical Care Medicine, Department of Internal Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Francesca Levi-Schaffer (F)

Pharmacology and Experimental Therapeutics Unit, School of Pharmacy, Institute for Drug Research, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel. Electronic address: francescal@ekmd.huji.ac.il.

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Classifications MeSH