Phenotypical and Functional Characterization of Neutrophils in Two Pyrin-Associated Auto-inflammatory Diseases.


Journal

Journal of clinical immunology
ISSN: 1573-2592
Titre abrégé: J Clin Immunol
Pays: Netherlands
ID NLM: 8102137

Informations de publication

Date de publication:
07 2021
Historique:
received: 05 02 2021
accepted: 23 02 2021
pubmed: 6 3 2021
medline: 4 2 2022
entrez: 5 3 2021
Statut: ppublish

Résumé

Familial Mediterranean Fever (FMF) and Pyrin-Associated Autoinflammation with Neutrophilic Dermatosis (PAAND) are clinically distinct autoinflammatory disorders caused by mutations in the pyrin-encoding gene MEFV. We investigated the transcriptional, phenotypical, and functional characteristics of patient neutrophils to explore their potential role in FMF and PAAND pathophysiology. RNA sequencing was performed to discover transcriptional aberrancies. The phenotypical features, degranulation properties, and phagocytic capacity of neutrophils were assessed by flow cytometry. Production of reactive oxygen species (ROS), myeloperoxidase (MPO) release, and chemotactic responses were investigated via chemiluminescence, ELISA, and Boyden chamber assays, respectively. Neutrophils from PAAND and FMF patients showed a partially overlapping, activated gene expression profile with increased expression of S100A8, S100A9, S100A12, IL-4R, CD48, F5, MMP9, and NFKB. Increased MMP9 and S100A8/A9 expression levels were accompanied by high plasma concentrations of the encoded proteins. Phenotypical analysis revealed that neutrophils from FMF patients exhibited an immature character with downregulation of chemoattractant receptors CXCR2, C5aR, and BLTR1 and increased expression of Toll-like receptor 4 (TLR4) and TLR9. PAAND neutrophils displayed an increased random, but reduced CXCL8-induced migration. A tendency for enhanced random migration was observed for FMF neutrophils. PAAND neutrophils showed a moderately but significantly enhanced phagocytic activity as opposed to neutrophils from FMF patients. Neutrophils from both patient groups showed increased MPO release and ROS production. Neutrophils from patients with FMF and PAAND, carrying different mutations in the MEFV gene, share a pro-inflammatory phenotype yet demonstrate diverse features, underscoring the distinction between both diseases.

Identifiants

pubmed: 33666778
doi: 10.1007/s10875-021-01008-4
pii: 10.1007/s10875-021-01008-4
doi:

Substances chimiques

Calgranulin A 0
Calgranulin B 0
Cytokines 0
MEFV protein, human 0
Pyrin 0
S100A8 protein, human 0
S100A9 protein, human 0
Peroxidase EC 1.11.1.7
MMP9 protein, human EC 3.4.24.35
Matrix Metalloproteinase 9 EC 3.4.24.35

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1072-1084

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Auteurs

Bert Malengier-Devlies (B)

Laboratory of Immunobiology, Rega Institute, KU Leuven, Leuven, Belgium.

Mieke Metzemaekers (M)

Laboratory of Molecular Immunology, Rega Institute, KU Leuven, Leuven, Belgium.

Mieke Gouwy (M)

Laboratory of Molecular Immunology, Rega Institute, KU Leuven, Leuven, Belgium.

Erika Van Nieuwenhove (E)

Division of Pediatric Rheumatology, Department Pediatrics, University Hospitals Leuven, Leuven, Belgium.

Albrecht Betrains (A)

Laboratory of Clinical Infectious and Inflammatory Disorders, KU Leuven, Leuven, Belgium.
European Reference Network for Rare Immunodeficiency, Autoinflammatory and Autoimmune Diseases (RITA), University Hospital Leuven, Leuven, Belgium.

Maaike Cockx (M)

Laboratory of Molecular Immunology, Rega Institute, KU Leuven, Leuven, Belgium.

Lotte Vanbrabant (L)

Laboratory of Molecular Immunology, Rega Institute, KU Leuven, Leuven, Belgium.

Noëmie Pörtner (N)

Laboratory of Molecular Immunology, Rega Institute, KU Leuven, Leuven, Belgium.

Jurgen Vercauteren (J)

Laboratory of Clinical en Epidemiological Virology, KU Leuven, Leuven, Belgium.

Lien De Somer (L)

Laboratory of Immunobiology, Rega Institute, KU Leuven, Leuven, Belgium.
Division of Pediatric Rheumatology, Department Pediatrics, University Hospitals Leuven, Leuven, Belgium.
European Reference Network for Rare Immunodeficiency, Autoinflammatory and Autoimmune Diseases (RITA), University Hospital Leuven, Leuven, Belgium.

Sofie Struyf (S)

Laboratory of Molecular Immunology, Rega Institute, KU Leuven, Leuven, Belgium.

Steven Vanderschueren (S)

Laboratory of Clinical Infectious and Inflammatory Disorders, KU Leuven, Leuven, Belgium.
European Reference Network for Rare Immunodeficiency, Autoinflammatory and Autoimmune Diseases (RITA), University Hospital Leuven, Leuven, Belgium.
Division of General Internal Medicine, University Hospitals Leuven, Leuven, Belgium.

Ellen De Langhe (E)

European Reference Network for Rare Immunodeficiency, Autoinflammatory and Autoimmune Diseases (RITA), University Hospital Leuven, Leuven, Belgium.
Division of Rheumatology, University Hospitals Leuven, Leuven, Belgium.
Laboratory of Tissue Homeostasis and Disease, KU Leuven, Leuven, Belgium.

Paul Proost (P)

Laboratory of Molecular Immunology, Rega Institute, KU Leuven, Leuven, Belgium. paul.proost@kuleuven.be.

Patrick Matthys (P)

Laboratory of Immunobiology, Rega Institute, KU Leuven, Leuven, Belgium.

Carine Wouters (C)

Laboratory of Immunobiology, Rega Institute, KU Leuven, Leuven, Belgium. carine.wouters@uzleuven.be.
Division of Pediatric Rheumatology, Department Pediatrics, University Hospitals Leuven, Leuven, Belgium. carine.wouters@uzleuven.be.
European Reference Network for Rare Immunodeficiency, Autoinflammatory and Autoimmune Diseases (RITA), University Hospital Leuven, Leuven, Belgium. carine.wouters@uzleuven.be.

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