Interleukin-17 drives pulmonary eosinophilia following repeated exposure to Aspergillus fumigatus conidia.
Infect Immun
; 80(4): 1424-36, 2012 Apr.
Article
em En
| MEDLINE
| ID: mdl-22252873
ABSTRACT
Previous research in our laboratory has demonstrated that repeated intranasal exposure to Aspergillus fumigatus conidia in C57BL/6 mice results in a chronic pulmonary inflammatory response that reaches its maximal level after four challenges. The inflammatory response is characterized by eosinophilia, goblet cell metaplasia, and T helper T(H)2 cytokine production, which is accompanied by sustained interleukin-17 (IL-17) expression that persists even after the T(H)2 response has begun to resolve. T(H)17 cells could develop in mice deficient in gamma interferon (IFN-γ), IL-4, or IL-10. In the lungs of IL-17 knockout mice repeatedly challenged with A. fumigatus conidia, inflammation was attenuated (with the most significant decrease occurring in eosinophils), conidial clearance was enhanced, and the early transient peak of CD4(+) CD25(+) FoxP3(+) cells blunted. IL-17 appeared to play only a minor role in eosinophil differentiation in the bone marrow but a central role in eosinophil extravasation from the blood into the lungs. These observations point to an expanded role for IL-17 in driving T(H)2-type inflammation to repeated inhalation of fungal conidia.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Eosinofilia Pulmonar
/
Aspergillus fumigatus
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Esporos Fúngicos
/
Interleucina-17
/
Aspergilose Pulmonar
Limite:
Animals
Idioma:
En
Revista:
Infect Immun
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
Estados Unidos