BACKGROUND: Bronchial asthma is a complex genetic disorder. Although serum IgE level and bronchial hyperresponsiveness are well known to be under genetic control, the influence of genetic factors on basophil releasability has been seldom studied. OBJECTIVE: The present study was carried out to investigate whether genetic factors may influence the basophil histamine releasability. MATERIALS AND METHODS: We studied 50 children, 32 with atopic asthma (AA) and 18 normal control (NC), and their parents. Suspensions of leukocytes were isolated and stimulated with Ca ionophore and anti-IgE antibody. Then, histamine in the supernatant was as-sayed by an automated fluorometric analyzer. RESULTS: Among the probands, AA children had a significantly higher anti-IgE induced histamine release than NC children. In contrast, Ca ionophore-induced histamine release was similar between the two groups. Ca ionophore-induced or anti-IgE-induced histamine release was not significantly different between parents of AA children and those of NC children. However, the maximal histamine release by Ca ionophore in parents had a significant correlation with that of probands, whereas the values by anti-IgE were not correlated between probands and their parents. CONCLUSION: We confirmed that basophils from patients with atopic asthma are characterized by a specific increase in IgE-mediated histamine release. The significant correlation of Ca ionophore-induced maximal histamine release between children and their parents suggests that genetic factors may play an important role in the control of non-IgE-mediated relessability from basophils.
Asthma ; Basophils* ; Child ; Genetics ; Histamine Release ; Histamine* ; Humans ; Immunoglobulin E ; Leukocytes ; Parents ; Suspensions

The pathogenic mechanism of ASA-induced urticaria/angioedema (AIU) is still poorly understood, but it has been known that histamine releasing by cutaneous mast cell activation is considered to be an important role. Considering the importance of histamine in AIU, we speculated that a genetic abnormality of histamine-related genes such as a high-affinity IgE receptor, a metabolic enzyme of histamines and histamine receptors, may be involved in the development of AIU. Enrolled in the study were 110 patients with AIU, 53 patients without ASA hypersensitivity who had various drug allergies presenting as exanthematous skin symptoms, and 99 normal healthy controls (NC). Eleven single nucleotide polymorphisms (SNPs) of the beta chain of the high-affinity IgE receptor (FCER1B) and three histamine-related genes-histamine N-methyltransferase (HNMT), histamine H1 receptor (HRH1), histamine H2 receptor (HRH2)-were screened using the SNP-IT assay based on a single base extension method. No significant differences were observed in allele and genotype frequencies, and haplotype frequencies of all the SNPs of FCER1B, HNMT, HRH1, and HRH2 among the three groups (p>0.05, respectively). These results suggest that the polymorphisms of FCER1B and the three histamine-related genes may not contribute to the development of AIU phenotype in the Korean population.
Adult ; Alleles ; Angioneurotic Edema/chemically induced/*genetics/metabolism ; Aspirin ; Female ; Gene Frequency ; Genotype ; Haplotypes ; Histamine/*metabolism ; Histamine Release/genetics ; Humans ; Linkage Disequilibrium ; Male ; Middle Aged ; *Polymorphism, Single Nucleotide ; Receptors, IgE/*genetics ; Research Support, Non-U.S. Gov't ; Urticaria/chemically induced/*genetics/metabolism