| Autor: |
Xia, Jin–Qi, Rickaby, David A., Kelly, Kevin J., Choi, Hongyung, Dawson, Christopher A., Kurup, Viswanath P. |
| Předmět: |
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| Zdroj: |
International Archives of Allergy & Immunology; 1999, Vol. 118 Issue 1, p23-29, 7p |
| Abstrakt: |
Background: Natural rubber latex has been reported as a major cause of allergy and asthma in a number of individuals. One of the occupational groups most affected by latex allergy are the health care workers who are frequently exposed to natural rubber latex products in their patient care activities. The immunopathogenesis of latex allergy is not well understood. In order to understand the immune mechanism in latex allergy, we have developed a mouse model of latex allergy. Methods: Both wild–type and IL–4 knockout BALB/c mice were challenged intranasally with latex proteins and their immune responses, lung pathology, and airway reactivity were evaluated. Results: The total serum IgE and latex specific IgE, IgG1, and peripheral blood and lung eosinophil levels in wild type BALB/c mice were enhanced by the latex exposure, while no IgE or eosinophil were detected in IL–4 knockout mice. Latex–specific IgG1 levels in the sera were lower in IL–4 knockout animals compared to wild mice. However, latex–specific IgG2a antibody was higher in all the IL–4 knockout mice compared to wild type mice. Both the wild type and IL–4 knockout animals developed increased airway resistance after antigen challenge when compared to control animals, although the airway resistance response of IL–4 knockout animals was attenuated compared to the wild–type animals. The histology of the lungs of these two groups of animals was similar. Conclusion: In spite of the differences in the immune responses in the two groups of mice, there were comparable lung inflammatory responses, suggesting a multifactorial pathogenetic mechanism. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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