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Increased levels of IgG to cytokeratin 19 in sera of patients with toluene diisocyanate-induced asthma.

Authors
Choi, JH; Nahm, DH; Kim, SH; Kim, YS; Suh, CH; Park, HS; Ahn, SW
Citation
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology, 93(3):293-298, 2004
Journal Title
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
ISSN
1081-12061534-4436
Abstract
BACKGROUND: Inhaled isocyanate binds with cytokeratin (CK) of the epithelial cells, which could induce immune responses.



OBJECTIVE: To elucidate the possible existence of an isocyanate-induced, asthma-associated autoantigen from the bronchial epithelial cells, which may be associated with toluene diisocyanate (TDI)-induced asthma development.



METHODS: We cultured bronchial epithelial cells with incubation of TDI-human serum albumin (HSA) conjugate. Gene expression profiles of cultured epithelial cells were analyzed using a microarray technique. CK19 protein expression within the epithelial cells was confirmed by IgG immunoblot using monoclonal antibody to CK19. Serum IgG to CK19 and specific IgG and IgE antibodies to TDI-HSA conjugate were detected by enzyme-linked immunosorbent assay in 68 TDI asthma patients (group 1) and compared with 40 allergic asthma patients (group 2) and 80 unexposed healthy controls (group 3).



RESULTS: After TDI exposure, increased expression of CK19 and CK14 genes from the culture bronchial epithelial cells was noted using microarray analysis. IgG immunoblot analysis confirmed increased expression of CK19 after the TDI exposure. The levels of serum IgG to CK19 were significantly higher in the TDI asthma group than in groups 2 and 3 (P=.008). The prevalence of IgG to CK19 was significantly higher in group 1 (38.2%) than group 2 (22.5%) or group 3 (1.3%) (P=.008). Significant associations were noted between IgG to CK19 and specific IgG to TDI-HSA conjugate and transglutaminase (P=.02) but not with specific IgE to TDI-HSA conjugate.



CONCLUSION: We suggest that TDI exposure can augment CK19 expression from the bronchial epithelial cell, which may involve immune responses as an autoantigen to induce airway inflammation in TDI-induced asthma.
MeSH terms
AdultAllergens/adverse effects/diagnostic useAntibody SpecificityAsthma/blood/chemically induced/*immunologyAutoantibodies/blood/*immunologyAutoantigens/drug effects/*immunologyBronchi/cytologyBronchial Provocation TestsCell Line, Transformed/drug effectsCells, CulturedCoculture TechniquesEnzyme-Linked Immunosorbent AssayEpithelial Cells/drug effects/metabolismFemaleGene Expression ProfilingHumansImmunoconjugates/pharmacologyImmunoglobulin E/blood/immunologyImmunoglobulin G/blood/*immunologyKeratins/drug effects/*immunologyMaleMethacholine Chloride/diagnostic useMiddle AgedOligonucleotide Array Sequence AnalysisRNA, Messenger/analysisSerum Albumin/pharmacologyToluene 2,4-Diisocyanate/*adverse effects/diagnostic use/pharmacokinetics
DOI
10.1016/S1081-1206(10)61504-9
PMID
15478392
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
Journal Papers > Research Organization > Regional Clinical Trial Center
Journal Papers > School of Medicine / Graduate School of Medicine > Rheumatology
AJOU Authors
남, 동호김, 승현서, 창희박, 해심
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