IL-1R1-MyD88 axis elicits papain-induced lung inflammation.
Eur J Immunol
; 46(11): 2531-2541, 2016 11.
Article
em En
| MEDLINE
| ID: mdl-27569535
ABSTRACT
Allergic asthma is characterized by a strong Th2 response with inflammatory cell recruitment and structural changes in the lung. Papain is a protease allergen disrupting the airway epithelium triggering a rapid inflammation with eosinophilia mediated by innate lymphoid cell activation (ILC2) and leading to a Th2 immune response. In this study, we focused on inflammatory responses to a single exposure to papain and showed that intranasal administration of papain results in the recruitment of inflammatory cells, including neutrophils and eosinophils with a rapid production of IL-1α, IL-1ß, and IL-33. The inflammatory response is abrogated in the absence of IL-1R1 and MyD88. To decipher the cell type(s) involved in MyD88-dependent IL-1R1/MyD88 signaling, we used new cell-specific MyD88-deficient mice and found that the deletion of MyD88 signaling in single cell types such as T cells, epithelial cells, CD11c-positive or myeloid cells leads to only a partial inhibition compared to complete absence of MyD88, suggesting that several cell types contribute to the response. Importantly, the inflammatory response is largely ST2 and IL-36R independent. In conclusion, IL-1R1 signaling via MyD88 is critical for the first step of inflammatory response to papain.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Pneumonia
/
Alérgenos
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Papaína
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Fator 88 de Diferenciação Mieloide
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Receptores Tipo I de Interleucina-1
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Imunidade Inata
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Pulmão
Limite:
Animals
Idioma:
En
Revista:
Eur J Immunol
Ano de publicação:
2016
Tipo de documento:
Article