Nocturnal asthma is affected by genetic interactions between RORA and NPSR1.


Journal

Pediatric pulmonology
ISSN: 1099-0496
Titre abrégé: Pediatr Pulmonol
Pays: United States
ID NLM: 8510590

Informations de publication

Date de publication:
06 2019
Historique:
received: 23 09 2018
revised: 17 12 2018
accepted: 04 02 2019
pubmed: 31 3 2019
medline: 18 3 2020
entrez: 31 3 2019
Statut: ppublish

Résumé

Neuropeptide S Receptor 1 ( NPSR1) and Retinoid Acid Receptor-Related Orphan Receptor Alpha (RORA ) interact biologically, are both known candidate genes for asthma, and are involved in controlling circadian rhythm. Thus, we assessed (1) whether interactions between RORA and NPSR1 specifically affect the nocturnal asthma phenotype and (2) how this may differ from other asthma phenotypes. Interaction effects between 24 single-nucleotide polymorphisms (SNPs) in RORA and 35 SNPs in NPSR1 on asthma and nocturnal asthma symptoms were determined in 1432 subjects (763 asthmatics [192 with nocturnal asthma symptoms]; 669 controls) from the Multicenter Asthma Genetic in Childhood/International Study of Asthma and Allergies in Childhood studies. The results were validated and extended in children from the Manchester Asthma and Allergy Study (N = 723) and the Children Allergy Milieu Stockholm and Epidemiological cohort (N = 1646). RORA* NPSR1 interactions seemed to affect both asthma and nocturnal asthma. In stratified analyses, however, interactions mainly affected nocturnal asthma and less so asthma without nocturnal symptoms or asthma severity. Results were replicated in two independent cohorts and seemed to remain constant over time throughout youth. RORA* NPSR1 interactions appear to be involved in mechanisms specific for nocturnal asthma. In contrast to previous studies focusing on the role of beta 2 receptor polymorphisms in nocturnal asthma as a feature of asthma control or severity in general, our data suggest that changes in circadian rhythm control are associated with nighttime asthma symptoms.

Sections du résumé

BACKGROUND
Neuropeptide S Receptor 1 ( NPSR1) and Retinoid Acid Receptor-Related Orphan Receptor Alpha (RORA ) interact biologically, are both known candidate genes for asthma, and are involved in controlling circadian rhythm. Thus, we assessed (1) whether interactions between RORA and NPSR1 specifically affect the nocturnal asthma phenotype and (2) how this may differ from other asthma phenotypes.
METHODS
Interaction effects between 24 single-nucleotide polymorphisms (SNPs) in RORA and 35 SNPs in NPSR1 on asthma and nocturnal asthma symptoms were determined in 1432 subjects (763 asthmatics [192 with nocturnal asthma symptoms]; 669 controls) from the Multicenter Asthma Genetic in Childhood/International Study of Asthma and Allergies in Childhood studies. The results were validated and extended in children from the Manchester Asthma and Allergy Study (N = 723) and the Children Allergy Milieu Stockholm and Epidemiological cohort (N = 1646).
RESULTS
RORA* NPSR1 interactions seemed to affect both asthma and nocturnal asthma. In stratified analyses, however, interactions mainly affected nocturnal asthma and less so asthma without nocturnal symptoms or asthma severity. Results were replicated in two independent cohorts and seemed to remain constant over time throughout youth.
CONCLUSION
RORA* NPSR1 interactions appear to be involved in mechanisms specific for nocturnal asthma. In contrast to previous studies focusing on the role of beta 2 receptor polymorphisms in nocturnal asthma as a feature of asthma control or severity in general, our data suggest that changes in circadian rhythm control are associated with nighttime asthma symptoms.

Identifiants

pubmed: 30927345
doi: 10.1002/ppul.24292
doi:

Substances chimiques

NPSR1 protein, human 0
Nuclear Receptor Subfamily 1, Group F, Member 1 0
RORA protein, human 0
Receptors, G-Protein-Coupled 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

847-857

Subventions

Organisme : Medical Research Council
ID : MR/L012693/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0601361
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/K002449/1
Pays : United Kingdom

Informations de copyright

© 2019 Wiley Periodicals, Inc.

Auteurs

Vincent D Gaertner (VD)

Department of Pediatric Pneumology and Allergy, University Children's Hospital Regensburg (KUNO), Regensburg, Germany.

Sven Michel (S)

Department of Pediatric Pneumology and Allergy, University Children's Hospital Regensburg (KUNO), Regensburg, Germany.

John A Curtin (JA)

Division of Infection Immunity and Respiratory Medicine, School of Biological Sciences, The University of Manchester, Manchester Academic Health Science Centre, and Manchester University NHS Foundation Trust, Manchester, UK.

Ville Pulkkinen (V)

Heart and Lung Center, Division of Pulmonary Medicine, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.

Nathalie Acevedo (N)

Department of Clinical Science and Education, Karolinska Institutet, Stockholm, Sweden.
Institute for Immunological Research, University of Cartagena, Cartagena, Colombia.

Cilla Söderhäll (C)

Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Department of Women´s and Children's Health, Karolinska Institutet, Stockholm, Sweden.

Andrea von Berg (A)

Children's Department, Research Institute for the Prevention of Allergic Diseases, Marien-Hospital, Wesel, Germany.

Albrecht Bufe (A)

Department of Experimental Pneumology, Ruhr-University, Bochum, Germany.

Otto Laub (O)

Kinder- und Jugendarztpraxis Laub, Rosenheim, Germany.

Ernst Rietschel (E)

Faculty of Medicine, University Children's Hospital, University of Cologne, Cologne, Germany.

Andrea Heinzmann (A)

Center for Pediatrics, Department of General Pediatrics, Adolescent Medicine and Neonatology, Faculty of Medicine, Medical Center - University of Freiburg, University of Freiburg, Freiburg im Breisgau, Germany.

Burkhard Simma (B)

Children's Department, University Teaching Hospital, Landeskrankenhaus Feldkirch, Feldkirch, Austria.

Christian Vogelberg (C)

University Children's Hospital, Technical University Dresden, Dresden, Germany.

Göran Pershagen (G)

Institute of Environmental Medicine, Karolinska Institutet and Centre for Occupational and Environmental Medicine, Stockholm County Council, Stockholm, Sweden.

Erik Melén (E)

Institute of Environmental Medicine, Karolinska Institutet and Centre for Occupational and Environmental Medicine, Stockholm County Council, Stockholm, Sweden.
Sachs' Children and Youth Hospital, Södersjukhuset, Stockholm, Sweden.

Angela Simpson (A)

Division of Infection Immunity and Respiratory Medicine, School of Biological Sciences, The University of Manchester, Manchester Academic Health Science Centre, and Manchester University NHS Foundation Trust, Manchester, UK.

Adnan Custovic (A)

Department of Paediatrics, Imperial College, London, UK.

Juha Kere (J)

Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Research Programs Unit, Program for Molecular Neurology, University of Helsinki, Folkhälsän Institute of Genetics, Helsinki, Finland.

Michael Kabesch (M)

Department of Pediatric Pneumology and Allergy, University Children's Hospital Regensburg (KUNO), Regensburg, Germany.
School of Basic & Medical Biosciences, King's College London, London, England.

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Classifications MeSH