Genetic susceptibility to severe asthma with fungal sensitization

Summary Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal sensitization (SAFS), used to denote this subgroup of asthma, respond to antifungal therapy. We have investigated 325 haplotype‐tagging SNPs i...

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Published inInternational journal of immunogenetics Vol. 44; no. 3; pp. 93 - 106
Main Authors Overton, N. L., Simpson, A., Bowyer, P., Denning, D. W.
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.06.2017
Subjects
Adult
Aged
allergy
Aspergillosis
Aspergillosis - complications
Aspergillosis - genetics
Aspergillosis - microbiology
Aspergillosis - pathology
Asthma
Asthma - complications
Asthma - genetics
Asthma - microbiology
Asthma - pathology
Atopy
CCL17 protein
Chemokine CCL17 - genetics
Chemokine CCL2 - genetics
disease association
disease association studies
Female
Genetic Association Studies
Genetic Predisposition to Disease
genetics
Genotype
Haplotypes
Humans
Interleukin 10
Interleukin-10 - genetics
Lectins, C-Type - genetics
Male
Mannose
Mannose-binding lectin
Mannose-Binding Lectin - genetics
Middle Aged
Monocyte chemoattractant protein 1
Plasminogen - genetics
polymorphism
Polymorphism, Single Nucleotide
Receptor, Adenosine A2A - genetics
Single-nucleotide polymorphism
TLR3 protein
TLR9 protein
Toll-Like Receptor 3 - genetics
Toll-Like Receptor 9 - genetics
Toll-like receptors
disease association studies
allergy
asthma
polymorphism
genetics
disease association
Online AccessGet full text
ISSN1744-3121
1744-313X
1744-313X
DOI10.1111/iji.12312

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Abstract Summary Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal sensitization (SAFS), used to denote this subgroup of asthma, respond to antifungal therapy. We have investigated 325 haplotype‐tagging SNPs in 22 candidate genes previously associated with aspergillosis in patients with SAFS, with comparisons in atopic asthmatics and healthy control patients, of whom 47 SAFS, 279 healthy and 152 atopic asthmatic subjects were genotyped successfully. Significant associations with SAFS compared with atopic asthma included Toll‐like receptor 3 (TLR3) (p = .009), TLR9 (p = .025), C‐type lectin domain family seven member A (dectin‐1) (p = .043), interleukin‐10 (IL‐10) (p = .0010), mannose‐binding lectin (MBL2) (p = .007), CC‐chemokine ligand 2 (CCL2) (2 SNPs, p = .025 and .041), CCL17 (p = .002), plasminogen (p = .049) and adenosine A2a receptor (p = .024). These associations differ from those found in ABPA in asthma, indicative of contrasting disease processes. Additional and broader genetic association studies in SAFS, combined with experimental work, are likely to contribute to our understanding of different phenotypes of problematic asthma.
AbstractList Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal sensitization ( SAFS ), used to denote this subgroup of asthma, respond to antifungal therapy. We have investigated 325 haplotype‐tagging SNP s in 22 candidate genes previously associated with aspergillosis in patients with SAFS , with comparisons in atopic asthmatics and healthy control patients, of whom 47 SAFS , 279 healthy and 152 atopic asthmatic subjects were genotyped successfully. Significant associations with SAFS compared with atopic asthma included Toll‐like receptor 3 ( TLR 3) ( p  = .009), TLR 9 ( p  = .025), C‐type lectin domain family seven member A (dectin‐1) ( p  = .043), interleukin‐10 ( IL ‐10) ( p  = .0010), mannose‐binding lectin ( MBL 2) ( p  = .007), CC ‐chemokine ligand 2 ( CCL 2) (2 SNP s, p  = .025 and .041), CCL 17 ( p  = .002), plasminogen ( p  = .049) and adenosine A2a receptor ( p  = .024). These associations differ from those found in ABPA in asthma, indicative of contrasting disease processes. Additional and broader genetic association studies in SAFS , combined with experimental work, are likely to contribute to our understanding of different phenotypes of problematic asthma.
Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal sensitization (SAFS), used to denote this subgroup of asthma, respond to antifungal therapy. We have investigated 325 haplotype-tagging SNPs in 22 candidate genes previously associated with aspergillosis in patients with SAFS, with comparisons in atopic asthmatics and healthy control patients, of whom 47 SAFS, 279 healthy and 152 atopic asthmatic subjects were genotyped successfully. Significant associations with SAFS compared with atopic asthma included Toll-like receptor 3 (TLR3) (p = .009), TLR9 (p = .025), C-type lectin domain family seven member A (dectin-1) (p = .043), interleukin-10 (IL-10) (p = .0010), mannose-binding lectin (MBL2) (p = .007), CC-chemokine ligand 2 (CCL2) (2 SNPs, p = .025 and .041), CCL17 (p = .002), plasminogen (p = .049) and adenosine A2a receptor (p = .024). These associations differ from those found in ABPA in asthma, indicative of contrasting disease processes. Additional and broader genetic association studies in SAFS, combined with experimental work, are likely to contribute to our understanding of different phenotypes of problematic asthma.Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal sensitization (SAFS), used to denote this subgroup of asthma, respond to antifungal therapy. We have investigated 325 haplotype-tagging SNPs in 22 candidate genes previously associated with aspergillosis in patients with SAFS, with comparisons in atopic asthmatics and healthy control patients, of whom 47 SAFS, 279 healthy and 152 atopic asthmatic subjects were genotyped successfully. Significant associations with SAFS compared with atopic asthma included Toll-like receptor 3 (TLR3) (p = .009), TLR9 (p = .025), C-type lectin domain family seven member A (dectin-1) (p = .043), interleukin-10 (IL-10) (p = .0010), mannose-binding lectin (MBL2) (p = .007), CC-chemokine ligand 2 (CCL2) (2 SNPs, p = .025 and .041), CCL17 (p = .002), plasminogen (p = .049) and adenosine A2a receptor (p = .024). These associations differ from those found in ABPA in asthma, indicative of contrasting disease processes. Additional and broader genetic association studies in SAFS, combined with experimental work, are likely to contribute to our understanding of different phenotypes of problematic asthma.
Summary Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal sensitization (SAFS), used to denote this subgroup of asthma, respond to antifungal therapy. We have investigated 325 haplotype-tagging SNPs in 22 candidate genes previously associated with aspergillosis in patients with SAFS, with comparisons in atopic asthmatics and healthy control patients, of whom 47 SAFS, 279 healthy and 152 atopic asthmatic subjects were genotyped successfully. Significant associations with SAFS compared with atopic asthma included Toll-like receptor 3 (TLR3) (p = .009), TLR9 (p = .025), C-type lectin domain family seven member A (dectin-1) (p = .043), interleukin-10 (IL-10) (p = .0010), mannose-binding lectin (MBL2) (p = .007), CC-chemokine ligand 2 (CCL2) (2 SNPs, p = .025 and .041), CCL17 (p = .002), plasminogen (p = .049) and adenosine A2a receptor (p = .024). These associations differ from those found in ABPA in asthma, indicative of contrasting disease processes. Additional and broader genetic association studies in SAFS, combined with experimental work, are likely to contribute to our understanding of different phenotypes of problematic asthma.
Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal sensitization (SAFS), used to denote this subgroup of asthma, respond to antifungal therapy. We have investigated 325 haplotype-tagging SNPs in 22 candidate genes previously associated with aspergillosis in patients with SAFS, with comparisons in atopic asthmatics and healthy control patients, of whom 47 SAFS, 279 healthy and 152 atopic asthmatic subjects were genotyped successfully. Significant associations with SAFS compared with atopic asthma included Toll-like receptor 3 (TLR3) (p = .009), TLR9 (p = .025), C-type lectin domain family seven member A (dectin-1) (p = .043), interleukin-10 (IL-10) (p = .0010), mannose-binding lectin (MBL2) (p = .007), CC-chemokine ligand 2 (CCL2) (2 SNPs, p = .025 and .041), CCL17 (p = .002), plasminogen (p = .049) and adenosine A2a receptor (p = .024). These associations differ from those found in ABPA in asthma, indicative of contrasting disease processes. Additional and broader genetic association studies in SAFS, combined with experimental work, are likely to contribute to our understanding of different phenotypes of problematic asthma.
Summary Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal sensitization (SAFS), used to denote this subgroup of asthma, respond to antifungal therapy. We have investigated 325 haplotype‐tagging SNPs in 22 candidate genes previously associated with aspergillosis in patients with SAFS, with comparisons in atopic asthmatics and healthy control patients, of whom 47 SAFS, 279 healthy and 152 atopic asthmatic subjects were genotyped successfully. Significant associations with SAFS compared with atopic asthma included Toll‐like receptor 3 (TLR3) (p = .009), TLR9 (p = .025), C‐type lectin domain family seven member A (dectin‐1) (p = .043), interleukin‐10 (IL‐10) (p = .0010), mannose‐binding lectin (MBL2) (p = .007), CC‐chemokine ligand 2 (CCL2) (2 SNPs, p = .025 and .041), CCL17 (p = .002), plasminogen (p = .049) and adenosine A2a receptor (p = .024). These associations differ from those found in ABPA in asthma, indicative of contrasting disease processes. Additional and broader genetic association studies in SAFS, combined with experimental work, are likely to contribute to our understanding of different phenotypes of problematic asthma.
Author Overton, N. L.
Bowyer, P.
Denning, D. W.
Simpson, A.
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  fullname: Denning, D. W.
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Issue 3
Keywords disease association studies
allergy
asthma
polymorphism
genetics
disease association
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
2017 John Wiley & Sons Ltd.
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Notes Funding information
The research leading to these results has received funding from the European Union's Seventh Framework Programme [FP7/2007‐2013] under grant agreement no HEALTH‐2010‐260338 (ALLFUN). Funding was also provided by the National Aspergillosis Centre, Medical Research Council (grant number MR/M02010X/1), Fungal Infection Trust, and JP Moulton Charitable Foundation and the North West Lung Centre Charity. This report is independent research supported by the National Institute for Health Research Clinical Research Facility at University Hospital of South Manchester NHS Foundation Trust. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health.
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2014; 43
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2012; 7
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2014; 78
2009; 103
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Snippet Summary Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal...
Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal...
Summary Severe asthma is problematic and its pathogenesis poorly understood. Fungal sensitization is common, and many patients with severe asthma with fungal...
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StartPage 93
SubjectTerms Adult
Aged
allergy
Aspergillosis
Aspergillosis - complications
Aspergillosis - genetics
Aspergillosis - microbiology
Aspergillosis - pathology
Asthma
Asthma - complications
Asthma - genetics
Asthma - microbiology
Asthma - pathology
Atopy
CCL17 protein
Chemokine CCL17 - genetics
Chemokine CCL2 - genetics
disease association
disease association studies
Female
Genetic Association Studies
Genetic Predisposition to Disease
genetics
Genotype
Haplotypes
Humans
Interleukin 10
Interleukin-10 - genetics
Lectins, C-Type - genetics
Male
Mannose
Mannose-binding lectin
Mannose-Binding Lectin - genetics
Middle Aged
Monocyte chemoattractant protein 1
Plasminogen - genetics
polymorphism
Polymorphism, Single Nucleotide
Receptor, Adenosine A2A - genetics
Single-nucleotide polymorphism
TLR3 protein
TLR9 protein
Toll-Like Receptor 3 - genetics
Toll-Like Receptor 9 - genetics
Toll-like receptors
Title Genetic susceptibility to severe asthma with fungal sensitization
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https://www.ncbi.nlm.nih.gov/pubmed/28371335
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