Publications by authors named "Inseon-S Choi"

Background/aims: Omalizumab is the first biologic known to be effective in patients with severe allergic asthma.

Methods: This study was conducted as a multicenter, single-group, open trial to evaluate the improvement in the quality of life with the additional administration of omalizumab for 24 weeks in Korean patients with severe persistent allergic asthma.

Results: Of the 44 patients, 31.

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Article Synopsis
  • A study confirmed that the ILVBL gene on chromosome 19p13.1 is linked to aspirin-exacerbated respiratory disease (AERD) and how much lung function declines after aspirin is given.
  • Researchers recruited 141 AERD patients and 995 aspirin-tolerant asthmatics, examining specific genetic variants called single nucleotide polymorphisms (SNPs) in the ILVBL gene.
  • Out of nine SNPs studied, seven were significantly associated with AERD risk, with five SNPs showing strong links and one (rs1468198) also linked to lung function changes, suggesting these SNPs might serve as genetic markers for AERD.
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Purpose: Inhalant allergen sensitization is one of the major factors involved in the pathogenesis of allergic respiratory diseases. However, the sensitization is determined by interactions between genetic and environmental factors. Thus, testing panels of inhalant allergens may differ among geographical areas.

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Purpose: We previously reported that the skin prick test was sensitive and the serum specific immunoglobulin E test was specific for predicting positive airway responses to house dust mites (HDMs) in patients with asthma. Because the nose and bronchus are one airway, the nasal provocation test would be more specific for predicting the bronchial responses to HDM than the skin test.

Methods: The allergy skin prick test and nasal and bronchial provocation tests using HDM (Dermatophagoides farinae) were performed in 41 young men (age, 19-28 years) who wanted military certification for asthma.

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Background: Aspirin-exacerbated respiratory disease (AERD) is characterized by a severe and sudden asthma attack after aspirin ingestion in patients with asthma. We studied associations with six common single nucleotide polymorphisms (SNP) of the gasdermin B gene (GSDMB).

Objective: DNA obtained from 572 patients with asthma (with AERD, n = 165; and with aspirin-tolerant asthma, n = 407) and 391 normal controls was subjected to genotyping of six SNPs of GSDMB.

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Background: We previously reported that as many as one third of hospitalized patients with asthma treated with a low to medium daily dose of inhaled steroids (ICSs) for an average of 4.5 years showed adrenal insufficiency (AI).

Objective: To re-examine this issue in consecutive outpatients with asthma because of possible subject selection bias.

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Background/aims: Mucosal immunoglobulin A (IgA) may prevent the entrance of allergens. This study examined the relationship between serum IgA levels (within the normal range) and sensitization to house dust mites (HDM) or airway hyper-responsiveness (AHR).

Methods: The clinical records of 1,136 adult patients with suspected asthma, for whom test data for serum IgA level and methacholine-AHR were available, were reviewed retrospectively.

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Aspirin-exacerbated respiratory disease (AERD) is one phenotype of asthma, often occurring in the form of a severe and sudden attack. Due to the time-consuming nature and difficulty of oral aspirin challenge (OAC) for AERD diagnosis, non-invasive biomarkers have been sought. The aim of this study was to identify AERD-associated exonic SNPs and examine the diagnostic potential of a combination of these candidate SNPs to predict AERD.

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Purpose: Endoplasmic reticulum (ER) stress has recently been observed to activate NF-kappaB and induce inflammatory responses such as asthma. Activating transcription factor 6β (ATF6B) is known to regulate ATFα-mediated ER stress response. The aim of this study is to investigate the associations of ATF6B genetic variants with aspirin-exacerbated respiratory disease (AERD) and its major phenotype, % decline of FEV1 by aspirin provocation.

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Member RAS oncogene family (RAB1A), a member of the RAS oncogene family, cycles between inactive GDP-bound and active GTP-bound forms regulating vesicle transport in exocytosis. Thus, functional alterations of the RAB1A gene may contribute to aspirin intolerance in asthmatic sufferers. To investigate the relationship between single-nucleotide polymorphisms (SNPs) in the RAB1A gene and aspirin-exacerbated respiratory disease (AERD), asthmatics (n=1197) were categorized into AERD and aspirin-tolerant asthma (ATA).

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Purpose: We previously demonstrated seasonal variation in sensitization to aeroallergens in a small group of patients with exercise-induced asthma. This study was performed to confirm the relationship in a much larger population.

Methods: The charts of 1,891 patients who received allergy skin prick tests were reviewed retrospectively.

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Immunoglobulin E (IgE) is one of the central players in asthma and allergic diseases. Although the serum IgE level, a useful endophenotype, is generally increased in patients with asthma, genetic factors influencing IgE regulation in asthma are still not fully understood. To identify the genetic variations associated with total serum and mite-specific IgEs in asthmatics, a genome-wide association study (GWAS) of 657,366 single nucleotide polymorphisms (SNPs) was performed in 877 Korean asthmatics.

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Background: Aspirin-exacerbated respiratory disease (AERD) is characterized by the development of airway obstruction in asthmatic individuals following the ingestion of aspirin or other nonsteroidal anti-inflammatory drugs. TAPBP (TAP-binding protein, tapasin) is upregulated by eicosanoids, which act as potent inflammatory molecules in aspirin-related reactions. Thus, functional alterations in the TAPBP gene may contribute toward AERD.

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Purpose: Aspirin exacerbated respiratory disease (AERD) results in a severe asthma attack after aspirin ingestion in asthmatics. The filamin A interacting protein 1 (FILIP1) may play a crucial role in AERD pathogenesis by mediating T cell activation and membrane rearrangement. We investigated the association of FILIP1 variations with AERD and the fall rate of forced expiratory volume in one second (FEV1).

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Aim: To investigate the association of single nucleotide polymorphisms (SNP) on IL17RA gene with Aspirin Exacerbated Respiratory Disease (AERD) and the functional effect of these variants on expression of IL17RA gene products.

Material & Methods: 15 SNPs of IL17RA gene were analyzed in 825 normal controls and 143 subjects with AERD and 411 with aspirin-tolerant asthma (ATA) and functionally characterized using measurement of protein and m-RNA expression.

Result: Minor alleles frequencies of the three SNPs (-1075 A>G, -947 A>G, -50 C>T) and one haplotype (BL1_ht1) were significantly lower in AERD compared to those in ATA (p(corr)=0.

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Article Synopsis
  • Aspirin-exacerbated respiratory disease (AERD) is a severe condition in which ingestion of NSAIDs like aspirin leads to a significant drop in lung function (FEV1), and its genetic underpinnings are not fully understood.
  • In a study involving Korean asthmatics, researchers conducted a genome-wide association study (GWAS) to identify genetic factors linked to AERD, analyzing samples from patients both with and without the condition.
  • The results identified a significant association between the HLA-DPB1 gene polymorphism (specifically rs1042151) and AERD susceptibility, highlighting its potential role as a key genetic risk factor among Korean asthmatics.
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The aim of the present study was to develop a diagnostic set of single-nucleotide polymorphisms (SNPs) for discriminating aspirin-exacerbated respiratory disease (AERD) from aspirin-tolerant asthma (ATA) using the genome-wide association study (GWAS) data; the GWAS data were filtered according to p-values and odds ratios (ORs) using PLINK software, and the 10 candidate SNPs most closely associated with AERD were selected, based on 100 AERD and 100 ATA subjects. Using multiple logistic regression and receiver-operating characteristic (ROC) curve analysis, eight SNPs were chosen as the best model for distinguishing between AERD and ATA. The relative risk for AERD in each subject was calculated based on the relative risk of each of the eight SNPs.

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Aspirin-exacerbated respiratory disease (AERD) is a respiratory disease characterized by acute bronchial responses upon the administration of non-steroidal anti‑inflammatory drugs (NSAIDs) and the immune response by mast cells is regarded as one of the noteworthy causes of AERD pathogenesis. The complement cascade is regarded as a key mechanism for clearing pathogens from the host. CD55 is one of the proteins involved in self-recognition, a central component of the complement system and autoimmunity.

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Aspirin-exacerbated respiratory disease (AERD) is a clinical syndrome characterized by bronchoconstriction after ingestion of nonsteroidal anti-inflammatory drugs including aspirin. The Ca concentration in bronchial epithelial cells is an important factor for bronchoconstriction. Human annexin A4 (ANXA4) is predominantly expressed in the secretory epithelia in the lung, stomach, intestine, and kidney.

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Purpose: Live/killed mycobacteria and culture supernatants can suppress asthmatic reactions. This study investigated whether mycobacterial secretory proteins have therapeutic effects on asthma.

Methods: Mycobacterium bovis bacille Calmette-Guérin (BCG; 2×10(5) CFUs) and mycobacterial secretory proteins (Ag85 complex, 38-kDa protein or MPB70; 4 or 20 µg) were administered intraperitoneally to female BALB/c mice with established airway hyperresponsiveness.

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Purpose: Exercise-induced bronchoconstriction (EIB) in patients with asthma occurs more frequently in winter than in summer. The concentration of house dust mite (HDM) allergens in beds also shows seasonal variation. This study examined the relationship between seasonal differences in the prevalence of EIB and sensitization to HDMs in patients with asthma.

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Aspirin exacerbated respiratory disease (AERD) is a clinical syndrome characterized by chronic rhinosinusitis with nasal polyposis and aspirin hypersensitivity. The aspirin-induced bronchospasm is mediated by mast cell and eosinophilic inflammation. Recently, it has been reported that the expression of discoidin, CUB and LCCL domain-containing protein 2 (DCBLD2) is up-regulated in lung cancers and is regulated by transcription factor AP-2 alpha (TFAP2A), a component of activator protein-2 (AP-2) that is known to regulate IL-8 production in human lung fibroblasts and epithelial cells.

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