Increased levels of Circulating Autoantibodies to Cultured Human Bronchial Epithelial Cell in Adult Patients with Nonatopic Asthma.
10.3346/jkms.2001.16.4.407
- Author:
Dong Ho NAHM
1
;
Min Jung SHIN
;
Hyunee YIM
;
Yup KANG
;
Dong Chul CHOI
;
Jin Kyoo KIM
;
Sun Sin KIM
;
Soo Keol LEE
;
Hae Sim PARK
Author Information
1. Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon. dhnahm@madang.ajou.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Asthma;
Autoantibodies
- MeSH:
Adult;
Asthma/*immunology;
Autoantibodies/*blood;
Bronchi/*immunology;
Cells, Cultured;
Epithelial Cells/immunology;
Human;
Hypersensitivity/immunology;
IgG/blood
- From:Journal of Korean Medical Science
2001;16(4):407-410
- CountryRepublic of Korea
- Language:English
-
Abstract:
The pathogenetic mechanism of nonatopic asthma has not yet been defined. The idea of a possible involvement of autoimmunity in the pathogenesis of nonatopic asthma has been proposed by earlier studies. To evaluate the possible involvement of autoimmune response against bronchial epithelial cell in the pathogenesis of nonatopic asthma, we measured circulating autoantibodies to cultured human bronchial epithelial cell (BEAS-2B cell line) using enzyme-linked immunosorbent assay. We used stored serum samples form 38 age-matched healthy controls, 26 adult patients with atopic asthma, 16 adult patients with nonatopic asthma, and 12 adult patients with systemic lupus erythematosus. Levels of IgG autoantibodies to bronchial epithelial cell were significantly higher in patients with nonatopic asthma (mean+/-SD of absorbance values; 0.135+/-0.030) and systemic lupus erythematosus (0.293+/-0.181) than in healthy controls (0.112+/-0.016) and patients with atopic asthma (0.116+/-0.031) (p<0.05). This study showed that levels of circulating IgG autoantibodies to bronchial epithelial cell were increased in adult patients with nonatopic asthma. Further studies are needed to evaluate the possible involvement of autoimmune mechanism in the pathogenesis of nonatopic asthma.
