1. ^*Departments of Industrial Hygiene and Toxicology and Occupational Medicine, Finnish Institute of Occupational Health, Helsinki, Finland
2. ^†Department of Pathology, Kymenlaakso Central Hospital, Kotka, Finland
3. ^‡Department of Pathology, Helsinki University Central Hospital, Helsinki, Finland
4. ^§Skin and Allergy Hospital, Helsinki University Central Hospital, Helsinki, Finland
5. ^¶Department of Dermatology, Tampere University and University Hospital, Tampere, Finland
6. ^#Laboratory of Immunobiology, National Public Health Institute, Helsinki, Finland

Correspondence: Harri Alenius, PhD, Laboratory of Immunotoxicology, Finnish Institute of Occupational Health, Topeliuksenkatu 41 aA, FIN-00250 Helsinki, Finland. Email: Harri.Alenius@ttl.fi

¹These authors contributed equally to this work.

Received 8 April 2005; Revised 6 June 2005; Accepted 21 June 2005; Published online 25 October 2005.

Abstract

As respiratory symptoms are common in addition to skin reactions in natural rubber latex allergy, we investigated the significance of different allergen exposure routes in the development of lung inflammation and airway hyperreactivity (AHR). Both intracutaneous (IC) and intraperitoneal (IP) exposure followed by airway challenge with latex proteins induced an influx of mononuclear cells and eosinophils to the lungs. AHR and lung mucus production increased significantly after IC and IP but not after intranasal (IN) exposure. Infiltration of inflammatory cells was associated with the induction of T-helper type 2 (Th2) cytokines and several CC chemokines. Only a marginal induction of these mediators was found after IN exposure. On the contrary, increased levels of transforming growth factor-1 and forkhead box 3 mRNA, markers of regulatory activities, were found in the lungs after IN but not after IC exposure. Finally, IC and IP, but not IN, latex exposure induced a striking increase in specific immunoglobulin E (IgE) levels. Cutaneous latex exposure in the absence of adjuvant followed by airway challenge induces a local Th2-dominated lung inflammation and a systemic IgE response. Cutaneous exposure to proteins eluting from latex products may therefore profoundly contribute to the development of asthma in latex allergy.