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Epicutaneous aeroallergen exposure induces systemic TH2 immunity that predisposes to allergic nasal responses. - PubMed - NCBI
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J Allergy Clin Immunol. 2006 Jul;118(1):62-9. Epub 2006 Jun 9.

Epicutaneous aeroallergen exposure induces systemic TH2 immunity that predisposes to allergic nasal responses.

Author information

1
Divisions of Allergy and Immunology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.

Abstract

BACKGROUND:

Atopic individuals are predisposed to mounting vigorous T(H)2-type immune responses to environmental allergens. The skin is often the first organ that manifests allergic disease and may provide an early entry point for antigen sensitization.

OBJECTIVE:

We sought to determine whether epicutaneous exposure to the aeroallergen Aspergillus fumigatus induces nasal allergic responses. Furthermore, we aimed to examine the mechanism involved.

METHODS:

Wild-type and signal transducer and activator of transcription 6 (STAT6)-deficient mice were exposed to epicutaneous A fumigatus and control antigen ovalbumin. Nasal inflammation and responsiveness to methacholine were monitored.

RESULTS:

Exposure to epicutaneous A fumigatus antigen induced a marked atopic dermatitis-like phenotype in a manner significantly more efficient than epicutaneous ovalbumin. A single A fumigatus intranasal challenge induced clinical nasal responses and hyperresponsiveness to methacholine in the nose as manifested by nasal symptoms, accompanied by allergic airway and nasal inflammation. Mechanistic analysis using gene-targeted mice revealed that the clinical nasal responses and hyperresponsiveness were STAT6-dependent. Although STAT6 was required for changes in nasal responses, it was not required for epicutaneous pathology except eosinophilia.

CONCLUSION:

Epicutaneous exposure to the aeroallergen A fumigatus potently primes for STAT6-dependent nasal responses. These results draw attention to the cooperative interaction between the nasal tract and skin.

CLINICAL IMPLICATIONS:

The skin is a potent site for antigen sensitization in the development of experimental allergic rhinitis.

PMID:
16815139
DOI:
10.1016/j.jaci.2006.04.046
[Indexed for MEDLINE]
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