Immune response and airway reactivity in wild and IL-4 knockout mice exposed to latex allergens

Background: Natural rubber latex has been reported as a major cause of alle rgy and asthma in a number of individuals. One of the occupational groups m ost affected by latex allergy are the health care workers who are frequentl y 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 mo use model of latex allergy. Methods: Both wild-type and IL-4 knockout BALB/ c mice were challenged intranasally with latex proteins and their immune re sponses, lung pathology, and airway reactivity were evaluated. Results: The total serum IgE and latex specific IgE, IgG1, and peripheral blood and lun g eosinophil levels in wild type BALB/c mice were enhanced by the latex exp osure, while no IgE or eosinophil were detected in IL-4 knockout mice. Late x-specific IgG1 levels in the sera were lower in IL-4 knockout animals comp ared 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 c hallenge when compared to central animals, although the airway resistance r esponse of IL-4 knockout animals was attenuated compared to the wild-type a nimals. The histology of the lungs of these two groups of animals was simil ar. Conclusion: In spite of the differences in the immune responses in the two groups of mice, there were comparable lung inflammatory responses, sugg esting a multifactorial pathogenetic mechanism.