We investigated the significance of different sensitization routes in the development of AHR and lung inflammation in natural rubber latex (NRL) allergy.

BALB/c mice were sensitized via intracutaneous (IC), intraperitoneal (IP) or intranasal (IN) routes with NRL followed by airway NRL challenge. AHR was measured by whole-body plethysmography. Lung inflammation was investigated from stained lung sections and from bronchoalveolar lavage. Lung cytokine and chemokine/receptor mRNA was measured by real-time PCR and serum antibodies by ELISA.

Significant increase in AHR and mucus production was found after IC and IP sensitization but not after IN sensitization. Both IC and IP sensitization induced an influx of eosinophils and lymphocytes to the lungs. Infiltration of inflammatory cells was associated with induction of Th2 cytokines and chemokines/receptors. Only marginal induction of these mediators was found after IN sensitization, however, increased levels of TGF-beta mRNA were found. Finally, IC and IP but not IN sensitization with NRL induced a striking increase in the total and specific IgE levels.

IC and IP sensitization elicits Th2-dominated airway inflammation and AHR in mice. Cutaneous route sensitization to proteins eluting from NRL products may therefore play an important role in the development of allergic asthma.