Park Cs

ADAM33 polymorphism : association with bronchial hyper-responsiveness in Korean asthmatics

Background A disintegrin and metalloprotease 33 (ADAM33) is expressed in the lung by fibroblasts and bronchial smooth muscle cells. Given its structure and cellular provenance, ADAM33 may be associated with airway remodelling and bronchial hyper‐responsiveness. Single nucleotide polymorphisms (SNPs) and haplotypes of the ADAM33 gene have previously been associated with asthma susceptibility in the Caucasian population.

Alpha‐T‐catenin (CTNNA3) gene was identified as a risk variant for toluene diisocyanate‐induced asthma by genome‐wide association analysis

Background Toluene diisocyanate (TDI) is the most important cause of occupational asthma, but the genetic mechanism of TDI‐induced asthma is still unknown.

Association of interleukin 18 (IL18) polymorphisms with specific IgE levels to mite allergens among asthmatic patients

Background:  Allergy is regarded as a multifactorial condition. Its onset and severity are influenced by both genetic and environmental factors. Identification of genetic factors involved in asthma development and related phenotypes is a major task in understanding the genetic background of asthma. The possible involvement of IL18 polymorphisms in asthma was examined in a Korean asthma cohort.

Nitric oxide metabolites in induced sputum: a marker of airway inflammation in asthmatic subjects

The role of nitric oxide (NO) needs to be further clarified in allergic inflammation. This study was designed to investigate the relationships between NO metabolites and eosinophil count, eosinophil cationic protein (ECP), interleukin (IL)‐5 in induced sputum from asthmatics.

A promoter nucleotide variant of the dendritic cell-specific DCNP1 associates with serum IgE levels specific for dust mite allergens among the Korean asthmatics

Dendritic cells (DCs), the most abundant antigen-presenting cells in the lung, have been drawing attention for their roles in specific allergic responses to aeroallergens with support of Th lymphocytes, and in persistent inflammatory changes in allergic asthma. To identify genetic factors that may be involved in the asthma susceptibility and development of the disease phenotypes, we examined association of DC-specific DCNP1 polymorphisms with the disease risk. The case–control study revealed association of the nucleotide variants with serum immunoglobulin E (IgE) levels specific for Dermatophagoides farinae (Der f 1) and Dermatophagoides pteronyssinus (Der p 1), major aeroallergens of dust mites, among subjects with asthma. In particular, the T-allele-carrying genotype frequencies for one of the variants (c.−1289C>T) located in the promoter region were found increased in the asthmatic group with low levels of the mite-specific IgE (odds ratio (OR)=0.63 (0.48–0.83) for Der p 1). Results from functional analyses indicated that the promoter variant would affect the gene expression by modulating DNA–protein interaction. We propose that the genetic polymorphism of DCNP1 may influence production of specific IgE by altering DC functions in the mite allergen presenting and/or processing. The functional relevance of the genetic variation would provide an important insight into the genetic basis of allergic response to the mite antigens.

Plasma protein profiles in early asthmatic responses to inhalation allergen challenge.

Although mediators, such as lipids, cytokines, and chemokines, are related to the appearance of an IPR, there has been no reliable indicator to predict conditions for the appearance of an IPR.

Relationship between neurokinin 2 receptor gene polymorphisms and serum vascular endothelial growth factor levels in patients with toluene diisocyanate-induced asthma

Background Among the various pathogenic mechanisms of toluene diisocyanate (TDI)‐induced asthma, a contribution from neurogenic inflammation has been suggested.

Bronchial hyperreactivity in patients with endobronchial tuberculosis

Some patients with endobronchial tuberculosis (EBTB) have wheeze on physical examination and normal chest PA, which mimic bronchial asthma. Non-specific bronchial challenge tests have been used to confirm the presence of bronchial hyperreactivity, which is a hallmark of bronchial asthma. To evaluate the effect of endobronchial tuberculous inflammation on bronchial responsiveness to histamine, the provocation concentrations of histamine required to reduce FEV1 by 20% of the pre-challenge baseline (PC20) were compared between patients with EBTB, patients with symptomatic bronchial asthma and normal, healthy controls. PC20 in EBTB patients (17.2 +/- 2.3 mg ml-1) and normal controls (19.5 +/- 1.4 mg ml-1) were significantly higher than in bronchial asthma patients (0.99 +/- 0.15 mg ml-1). PC20 in EBTB patients was not affected by disease location in the bronchial tree was not correlated with FVC or FEV1. In conclusion, one should consider the possibility of EBTB for differential diagnosis from bronchial asthma, if airway responsiveness appears normal in wheezy patients.

Genetic effect of single-nucleotide polymorphisms in the PPARGC1B gene on airway hyperreactivity in asthmatic patients.

Background Peroxisome proliferator‐activated receptor gamma coactivator 1 beta (PPARGC1B) is a co‐activator for intracellular receptors such as the estrogen receptor, PPAR, and glucocorticoid receptor, which are involved in asthma development.

Common promoter polymorphism in monocyte differentiation antigen CD14 is associated with serum triglyceride levels and body mass index in non-diabetic individuals

Aims  Growing evidence supports the hypothesis that chronic low‐grade inflammation related to innate immunity may play an important role in the pathophysiology of Type 2 diabetes mellitus (T2DM). The monocyte differentiation antigen CD14 gene (CD14) acts as the receptor for lipopolysaccharide (LPS) and augments monocyte/macrophage inflammatory responses.