Increased production of serum IgA-class antibody to lipid A in Kawasaki disease
Background : The etiology of Kawasaki disease (KD) remains unknown. To investigate whether a conventional bacterial antigen is involved in the pathogenesis of KD, we studied the serum response to lipopolysaccharide (LPS). Methods : We measured the serum levels of IgG‐, IgM‐ and IgA‐class antibodies...
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Published in | Pediatrics international Vol. 44; no. 1; pp. 5 - 11 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Science, Ltd
01.02.2002
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Subjects | |
Online Access | Get full text |
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Summary: | Background
: The etiology of Kawasaki disease (KD) remains unknown. To investigate whether a conventional bacterial antigen is involved in the pathogenesis of KD, we studied the serum response to lipopolysaccharide (LPS).
Methods
: We measured the serum levels of IgG‐, IgM‐ and IgA‐class antibodies (Ab) to lipid A, a toxic site of LPS, using enzyme‐linked immunosorbent assay in 20 patients with KD, 11 patients with Gram‐negative bacterial infection (GNBI), 27 healthy children and 12 healthy adults.
Results
: The serum levels of anti‐lipid A IgG, IgM and IgA tended to increase with advancing age in healthy children older than 6 months of age. The mean level of anti‐lipid A IgM in the acute phase of GNBI and the mean levels of anti‐lipid A IgM and IgA in the acute phase of KD were found to increase significantly, in comparison to the age‐matched controls. Furthermore, the mean level of anti‐lipid A IgA also showed a significant increase from the acute to the subacute phases of KD. Regarding the IgA‐subclass response, higher titers of anti‐lipid A specific Ab were seen in the IgA2 subclass than in the IgA1 subclass.
Conclusion
: These findings indicate that KD patients demonstrate an intense response to lipid A in the IgA, especially IgA2‐subclass, thus suggesting that an unusual activation of the mucosal immune response to a ubiquitous antigen derived from Gram‐negative bacteria may be involved in the pathogenesis of KD. |
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Bibliography: | ark:/67375/WNG-8ZWC5Z2H-L ArticleID:PED1506 istex:49D05DE68F2F4165778970E5A1F6C3467149FF55 |
ISSN: | 1328-8067 1442-200X |
DOI: | 10.1046/j.1442-200X.2002.01506.x |