Abstract
Purpose: A possible involvement of autoimmune mechanism in the pathogenesis of bronchial asthma has been proposed. Recently, alpha-enolase protein was identified as a major autoantigen recognized by circulating IgG autoantibodies in patients with severe asthma. To evaluate a possible pathogenetic significance of these autoantibodies in severe asthma, isotype (IgG, IgA, IgM, and IgE) and IgG subclass (IgG1, IgG2, IgG3, and IgG4) distributions of autoantibodies to recombinant human alpha-enolase protein were analyzed. Patients and Methods: We examined serum samples from 10 patients with severe asthma and 7 patients with mild-to-moderate asthma, and 5 healthy controls by immunoblot analysis. Severe asthma was defined as patients having at least 1 severe asthmatic exacerbation requiring an emergency department visit or admission in the last year despite continuous typical therapies. Results: IgG1 was the predominant IgG subclass antibody response to alpha-enolase protein in patients with severe asthma. IgG1 autoantibody to alpha-enolase protein was detected in 7 of 10 patients with severe asthma (70%), 1 of 7 patients with mild-to-moderate asthma (14.3%), and none of 5 healthy controls (0%) (chi-square test; p < 0.05). IgA, IgM, and IgE autoantibodies to alpha-enolase protein could not be detected in patients with severe asthma. Conclusion: IgG1 subclass was the predominant type of autoantibody response to alpha-enolase protein in patients with severe asthma, suggests a possibility of IgG1 autoantibody-mediated complement activation in the pathogenesis of severe asthma.
| Original language | English |
|---|---|
| Pages (from-to) | 923-930 |
| Number of pages | 8 |
| Journal | Yonsei Medical Journal |
| Volume | 49 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2008 Dec 1 |
| Externally published | Yes |
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Keywords
- Asthma
- Autoantibody
- IgE
- IgG
- IgG subclass
ASJC Scopus subject areas
- Medicine(all)
Cite this
Isotype and IgG subclass distribution of autoantibody response to alpha-enolase protein in adult patients with severe Asthma. / Lee, Hye Ah; Kwon, Byul; Hur, Gyu Young; Choi, Sung Jin; Nahm, Dong Ho; Park, Hae Sim.
In: Yonsei Medical Journal, Vol. 49, No. 6, 01.12.2008, p. 923-930.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Isotype and IgG subclass distribution of autoantibody response to alpha-enolase protein in adult patients with severe Asthma
AU - Lee, Hye Ah
AU - Kwon, Byul
AU - Hur, Gyu Young
AU - Choi, Sung Jin
AU - Nahm, Dong Ho
AU - Park, Hae Sim
PY - 2008/12/1
Y1 - 2008/12/1
N2 - Purpose: A possible involvement of autoimmune mechanism in the pathogenesis of bronchial asthma has been proposed. Recently, alpha-enolase protein was identified as a major autoantigen recognized by circulating IgG autoantibodies in patients with severe asthma. To evaluate a possible pathogenetic significance of these autoantibodies in severe asthma, isotype (IgG, IgA, IgM, and IgE) and IgG subclass (IgG1, IgG2, IgG3, and IgG4) distributions of autoantibodies to recombinant human alpha-enolase protein were analyzed. Patients and Methods: We examined serum samples from 10 patients with severe asthma and 7 patients with mild-to-moderate asthma, and 5 healthy controls by immunoblot analysis. Severe asthma was defined as patients having at least 1 severe asthmatic exacerbation requiring an emergency department visit or admission in the last year despite continuous typical therapies. Results: IgG1 was the predominant IgG subclass antibody response to alpha-enolase protein in patients with severe asthma. IgG1 autoantibody to alpha-enolase protein was detected in 7 of 10 patients with severe asthma (70%), 1 of 7 patients with mild-to-moderate asthma (14.3%), and none of 5 healthy controls (0%) (chi-square test; p < 0.05). IgA, IgM, and IgE autoantibodies to alpha-enolase protein could not be detected in patients with severe asthma. Conclusion: IgG1 subclass was the predominant type of autoantibody response to alpha-enolase protein in patients with severe asthma, suggests a possibility of IgG1 autoantibody-mediated complement activation in the pathogenesis of severe asthma.
AB - Purpose: A possible involvement of autoimmune mechanism in the pathogenesis of bronchial asthma has been proposed. Recently, alpha-enolase protein was identified as a major autoantigen recognized by circulating IgG autoantibodies in patients with severe asthma. To evaluate a possible pathogenetic significance of these autoantibodies in severe asthma, isotype (IgG, IgA, IgM, and IgE) and IgG subclass (IgG1, IgG2, IgG3, and IgG4) distributions of autoantibodies to recombinant human alpha-enolase protein were analyzed. Patients and Methods: We examined serum samples from 10 patients with severe asthma and 7 patients with mild-to-moderate asthma, and 5 healthy controls by immunoblot analysis. Severe asthma was defined as patients having at least 1 severe asthmatic exacerbation requiring an emergency department visit or admission in the last year despite continuous typical therapies. Results: IgG1 was the predominant IgG subclass antibody response to alpha-enolase protein in patients with severe asthma. IgG1 autoantibody to alpha-enolase protein was detected in 7 of 10 patients with severe asthma (70%), 1 of 7 patients with mild-to-moderate asthma (14.3%), and none of 5 healthy controls (0%) (chi-square test; p < 0.05). IgA, IgM, and IgE autoantibodies to alpha-enolase protein could not be detected in patients with severe asthma. Conclusion: IgG1 subclass was the predominant type of autoantibody response to alpha-enolase protein in patients with severe asthma, suggests a possibility of IgG1 autoantibody-mediated complement activation in the pathogenesis of severe asthma.
KW - Asthma
KW - Autoantibody
KW - IgE
KW - IgG
KW - IgG subclass
UR - http://www.scopus.com/inward/record.url?scp=58149470824&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=58149470824&partnerID=8YFLogxK
U2 - 10.3349/ymj.2008.49.6.923
DO - 10.3349/ymj.2008.49.6.923
M3 - Article
C2 - 19108015
AN - SCOPUS:58149470824
VL - 49
SP - 923
EP - 930
JO - Yonsei Medical Journal
JF - Yonsei Medical Journal
SN - 0513-5796
IS - 6
ER -