Mannose-Binding Lectin (MBL) and Gap Junction Protein Alpha 4 (GJA4) Gene Heterogeneity in Relation to Severity of Clinical Disease in Cystic Fibrosis.

bronchial inflammation cystic fibrosis delta F 508 homozygous gap junction protein alpha 4 (GJA4) gene-gene interaction mannose-binding lectin

Journal

Frontiers in bioscience (Landmark edition)
ISSN: 2768-6698
Titre abrégé: Front Biosci (Landmark Ed)
Pays: Singapore
ID NLM: 101612996

Informations de publication

Date de publication:
30 05 2022
Historique:
received: 30 12 2021
revised: 15 02 2022
accepted: 17 02 2022
entrez: 24 6 2022
pubmed: 25 6 2022
medline: 28 6 2022
Statut: ppublish

Résumé

Recently, we provided evidence that a single nucleotide polymorphism (SNP), rs41266431, on the gap junction protein alpha 4 (GJA4) gene, acts as a modifier for clinical disease severity in patients with cystic fibrosis (CF). These features are very similar to those of variants of the mannose-binding lectin (MBL). This study aimed to clarify whether the clinical disease phenotype associated with GJA4 variants is independent of MBL variants. One hundred and twelve patients with homozygous F508del (mean age, 27.6 years; m/f, 61/51) were recruited from the CF centers of Bonn, Frankfurt, and Amsterdam. A sequence analysis was performed for GJA4 and MBL. The clinical phenotype was assessed over three years using pulmonary function tests, body mass index, A clinically relevant SNP of GJA4 was identified by sequence analysis. Pulmonary function (FVC% pred, mean 78/85; The clinical disease phenotype associated with GJA4 variants is independent of MBL variants. MBL-sufficient variants were associated with superior BMI and a trend for better survival than MBL insufficient variants.

Sections du résumé

BACKGROUND
Recently, we provided evidence that a single nucleotide polymorphism (SNP), rs41266431, on the gap junction protein alpha 4 (GJA4) gene, acts as a modifier for clinical disease severity in patients with cystic fibrosis (CF). These features are very similar to those of variants of the mannose-binding lectin (MBL). This study aimed to clarify whether the clinical disease phenotype associated with GJA4 variants is independent of MBL variants.
METHODS
One hundred and twelve patients with homozygous F508del (mean age, 27.6 years; m/f, 61/51) were recruited from the CF centers of Bonn, Frankfurt, and Amsterdam. A sequence analysis was performed for GJA4 and MBL. The clinical phenotype was assessed over three years using pulmonary function tests, body mass index,
RESULTS
A clinically relevant SNP of GJA4 was identified by sequence analysis. Pulmonary function (FVC% pred, mean 78/85;
CONCLUSIONS
The clinical disease phenotype associated with GJA4 variants is independent of MBL variants. MBL-sufficient variants were associated with superior BMI and a trend for better survival than MBL insufficient variants.

Identifiants

pubmed: 35748244
pii: S2768-6701(22)00527-5
doi: 10.31083/j.fbl2706168
doi:

Substances chimiques

Connexins 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

168

Informations de copyright

© 2022 The Author(s). Published by IMR Press.

Déclaration de conflit d'intérêts

(1) Sabina Schmitt-Grohé is on the advisory committee of Vertex and has received a travel grant from Vertex (for ECFS 2019) and ERS (ERS Research Seminars). Moreover, she gave a talk to Vertex, participated in studies for the same, received a fee for a congress report (ECFS conference Liverpool 2019), and attended a vertex-sponsored conference (1.CF-Akademie, Schloss Hohenkammer). In addition, she got financial reimbursement for a talk for Deutsche CF Hilfe and received a personal fee for an expert opinion for the Institut für Qualität und Wirtschaftlichkeit im Gesundheitswesen.

Auteurs

Joern Pascal Laubach (JP)

University Children's Hospital Bonn, 53127 Bonn, Germany.

Michael Ludwig (M)

Department of Clinical Chemistry and Clinical Pharmacology, University Hospital Bonn, 53127 Bonn, Germany.

Tabea Horn (T)

University Children's Hospital Bonn, 53127 Bonn, Germany.

Olaf Eickmeier (O)

Department for Children and Adolescents, Division of Allergology, Pulmonology, and Cystic Fibrosis, Goethe-University, 60590 Frankfurt, Germany.

Christina Smaczny (C)

Christiane-Herzog CF-Ambulanz, Goethe-University, 60590 Frankfurt, Germany.

Ralf Schubert (R)

Department for Children and Adolescents, Division of Allergology, Pulmonology, and Cystic Fibrosis, Goethe-University, 60590 Frankfurt, Germany.

Stefan Zielen (S)

Department for Children and Adolescents, Division of Allergology, Pulmonology, and Cystic Fibrosis, Goethe-University, 60590 Frankfurt, Germany.

Christof Majoor (C)

Department of Respiratory Medicine, Amsterdam University Medical Centers (UMC), 1100 Amsterdam, The Netherlands.

Malik Aydin (M)

Laboratory of Experimental Pediatric Pneumology and Allergology, Center for Biomedical Education and Research, School of Life Sciences (ZBAF), Department of Human Medicine, Faculty of Health, Witten/Herdecke University, 58448 Witten, Germany.

Sabina Schmitt-Grohé (S)

University Children's Hospital Bonn, 53127 Bonn, Germany.
Department for Children and Adolescents, Division of Allergology, Pulmonology, and Cystic Fibrosis, Goethe-University, 60590 Frankfurt, Germany.

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