Cutaneous, but not airway, latex exposure induces allergic lung inflammation and airway hyperreactivity in mice.
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-beta1 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.
Lehto
Maili
M
Department of Industrial Hygiene and Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Haapakoski
Rita
R
Wolff
Henrik
H
Majuri
Marja-Leena
ML
Mäkelä
Mika J
MJ
Leino
Marina
M
Reunala
Timo
T
Turjanmaa
Kristiina
K
Palosuo
Timo
T
Alenius
Harri
H
D000279:Administration, Cutaneous; D000281:Administration, Intranasal; D000485:Allergens / Q000008:administration & dosage / Q000276:immunology*; D000818:Animals; D052179:Antigens, Plant; D019742:Chemokines, CC / Q000235:genetics / Q000378:metabolism; D004804:Eosinophils / Q000276:immunology; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007840:Latex / Q000008:administration & dosage / Q000276:immunology*; D020315:Latex Hypersensitivity / Q000276:immunology*; D008168:Lung / Q000276:immunology; D051379:Mice; D010940:Plant Proteins / Q000276:immunology; D011014:Pneumonia / Q000276:immunology*; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D012130:Respiratory Hypersensitivity / Q000276:immunology*; D012867:Skin / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1; D015854:Up-Regulation
D000485:Allergens; D052179:Antigens, Plant; D019742:Chemokines, CC; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; C097982:Hev b 6.01 protein, Hevea brasiliensis; D007840:Latex; D010940:Plant Proteins; D012333:RNA, Messenger; C508961:Tgfb1 protein, mouse; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D007073:Immunoglobulin E