MRGPRX2 and Immediate Drug Hypersensitivity: Insights From Cultured Human Mast Cells.


Journal

Journal of investigational allergology & clinical immunology
ISSN: 1018-9068
Titre abrégé: J Investig Allergol Clin Immunol
Pays: Spain
ID NLM: 9107858

Informations de publication

Date de publication:
21 Dec 2021
Historique:
pubmed: 1 8 2020
medline: 14 1 2022
entrez: 1 8 2020
Statut: ppublish

Résumé

Mast cell (MC) degranulation via activation of the Mas-related G protein-coupled receptor X2 (MRGPRX2) plays a key role in immediate drug hypersensitivity (IDH). However, data in humans are limited to observations in specific cell lines. Objective: To study the usefulness of silencing MRGPRX2 in human MCs with the aim of further unveiling the MRGPRX2 pathway in IDH. MCs were cultured from CD34+ progenitor cells obtained from peripheral blood (PBCMCs) and incubated with substance P (as a positive control), rocuronium, moxifloxacin, morphine, or amoxicillin. Immunophenotyping of the cells included flow cytometry and microscopy analyses of the expression of CD117, CD203c, and MRGPRX2. Intracellular calcium was measured using Fluo-4. Degranulation was analyzed by quantifying CD63 expression. For MRGPRX2 silencing, MCs were electroporated with Dicer small interference RNAs. Incubation of MCs with substance P, morphine, and moxifloxacin increased intracellular calcium levels and triggered MC degranulation, which, for the drugs, is almost completely abolished by selective MRGPRX2 silencing. Despite an increase in intracellular calcium in MRGPRX2+ cells, incubation with nontoxic concentrations of rocuronium does not result in degranulation of PBCMCs. Amoxicillin has no effect on PBCMCs. The use of MRGPRX2 silencing in human MCs can provide important insights into the role of MRGPRX2 in the pathogenesis of IDH. As induction of calcium signals does not necessarily translate into a secretory response, measurement of the degranulation reaction seems more meaningful in the context of drug testing.

Sections du résumé

BACKGROUND AND OBJECTIVES OBJECTIVE
Mast cell (MC) degranulation via activation of the Mas-related G protein-coupled receptor X2 (MRGPRX2) plays a key role in immediate drug hypersensitivity (IDH). However, data in humans are limited to observations in specific cell lines. Objective: To study the usefulness of silencing MRGPRX2 in human MCs with the aim of further unveiling the MRGPRX2 pathway in IDH.
METHODS METHODS
MCs were cultured from CD34+ progenitor cells obtained from peripheral blood (PBCMCs) and incubated with substance P (as a positive control), rocuronium, moxifloxacin, morphine, or amoxicillin. Immunophenotyping of the cells included flow cytometry and microscopy analyses of the expression of CD117, CD203c, and MRGPRX2. Intracellular calcium was measured using Fluo-4. Degranulation was analyzed by quantifying CD63 expression. For MRGPRX2 silencing, MCs were electroporated with Dicer small interference RNAs.
RESULTS RESULTS
Incubation of MCs with substance P, morphine, and moxifloxacin increased intracellular calcium levels and triggered MC degranulation, which, for the drugs, is almost completely abolished by selective MRGPRX2 silencing. Despite an increase in intracellular calcium in MRGPRX2+ cells, incubation with nontoxic concentrations of rocuronium does not result in degranulation of PBCMCs. Amoxicillin has no effect on PBCMCs.
CONCLUSION CONCLUSIONS
The use of MRGPRX2 silencing in human MCs can provide important insights into the role of MRGPRX2 in the pathogenesis of IDH. As induction of calcium signals does not necessarily translate into a secretory response, measurement of the degranulation reaction seems more meaningful in the context of drug testing.

Identifiants

pubmed: 32732181
doi: 10.18176/jiaci.0557
doi:

Substances chimiques

MRGPRX2 protein, human 0
Nerve Tissue Proteins 0
Receptors, G-Protein-Coupled 0
Receptors, Neuropeptide 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

489-499

Auteurs

J Elst (J)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, B.

V Sabato (V)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, B.
Department of Immunology, AZ Jan Palfijn Hospital Gent, Ghent, Belgium.

M A Faber (MA)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, B.

C H Bridts (CH)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, B.

C Mertens (C)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, B.

M Van Houdt (M)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, B.

A L Van Gasse (AL)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, B.
Department of Pediatrics, Faculty of Medicine and Health Sciences, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.

M M Hagendorens (MM)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, B.
Department of Pediatrics, Faculty of Medicine and Health Sciences, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.

V Van Tendeloo (V)

Laboratory of Experimental Haematology, Vaccine & Infectious Disease Institute (VAXINFECTIO), Faculty of Medicine and Health Science, University of Antwerp, Antwerp, Belgium.

M Maurer (M)

Dermatological Allergology, Allergie-Centrum-Charité, Department of Dermatology and Allergy, Charité - Universitätsmedizin Berlin, Berlin, Germany.

D Campillo-Davo (D)

Laboratory of Experimental Haematology, Vaccine & Infectious Disease Institute (VAXINFECTIO), Faculty of Medicine and Health Science, University of Antwerp, Antwerp, Belgium.

J P Timmermans (JP)

Laboratory of Cell Biology and Histology, Department of Veterinary Sciences, University of Antwerp, Antwerp, Belgium.

I Pintelon (I)

Laboratory of Cell Biology and Histology, Department of Veterinary Sciences, University of Antwerp, Antwerp, Belgium.

D G Ebo (DG)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Centre of Excellence, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium and Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, B.
Department of Immunology, AZ Jan Palfijn Hospital Gent, Ghent, Belgium.

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