Circulating Autoantibodies in Patients with Aspirin-intolerant Asthma: An Epiphenomenon Related to Airway Inflammation.
10.3346/jkms.2006.21.3.412
- Author:
Young Min YE
1
;
Dong Ho NAHM
;
Sang Ha KIM
;
Seung Hyun KIM
;
Jeong Hee CHOI
;
Chang Hee SUH
;
Hae Sim PARK
Author Information
1. Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Korea. hspark@ajou.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Aspirin;
Bronchoconstriction;
Aspirin-intolerant Asthma;
Autoantibodies;
Cytokeratin;
Keratin
- MeSH:
Middle Aged;
Male;
Keratins/chemistry;
Inflammation;
Humans;
Female;
*Drug Resistance;
Child;
Case-Control Studies;
Bronchi/*pathology;
Autoantibodies/*chemistry;
Asthma/*drug therapy/*immunology;
Aspirin/*pharmacology;
Anti-Inflammatory Agents, Non-Steroidal/pharmacology;
Aged
- From:Journal of Korean Medical Science
2006;21(3):412-417
- CountryRepublic of Korea
- Language:English
-
Abstract:
Several studies have suggested the involvement of an autoimmune mechanism in aspirin (ASA)-intolerant asthma. To test this hypothesis, we measured the levels of circulating autoantibodies, such as IgG and IgA to tissue transglutaminase (TGase), IgG to cytokeratins (CKs) 8, 18, and 19, Clq-binding immune complex (CIC), and antinuclear antibody (ANA), in the sera of 79 patients with ASA-intolerant asthma (Group I) and those of two control groups, consisting of 61 patients with ASA-tolerant asthma (Group II) and 88 healthy control subjects (Group III) by means of ELISA. Significantly higher prevalences of IgG antibodies to CK18 (13.9%) and CK19 (17.7%) were noted in Group I, as compared with Group III (p<0.05 for all) not with Group II. Regarding the prevalences of other autoantibodies, the levels of ANA (1.3%), IgG to TGase (3.8%), and CIC (24.7%) in Group I were not significantly different from those in Groups II and III. Significant correlations were found between positivities for the anti-CK18 and anti-CK19 autoantibodies and the PC20 methacholine values in the analysis of asthma Groups I and II vs. normal controls, (p=0.001 and p=0.003, respectively). Further studies are needed to explore the potential involvement of an autoantibody-mediated mechanism in the clinical manifestation of bronchial asthma.
