Toll-like receptor 4 agonists adsorbed to aluminium hydroxide adjuvant attenuate ovalbumin-specific allergic airway disease: role of MyD88 adaptor molecule and interleukin-12/interferon-gamma axis

Autor(es):Mostrar menos -

Bortolatto, J. ; Borducchi, E. ; Rodriguez, D. ; Keller, A. C. ; Faquim-Mauro, E. ^[1] ; Bortoluci, K. R. ; Mucida, D. ; Gomes, E. ; Christ, A. ; Schnyder-Candrian, S. ^[2] ; Schnyder, B. ^[2] ; Ryffel, B. ^[2] ; Russo, M. ^[3]

Afiliação do(s) autor(es)

^[1] Inst Butantan, Immunopathol Lab, Sao Paulo - Brazil

^[2] CNRS, F-45071 Orleans - France

^[3] Univ Sao Paulo, ICB IV, Dept Immunol, Inst Biomed Sci, BR-05508000 Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: CLINICAL AND EXPERIMENTAL ALLERGY; v. 38, n. 10, p. 1668-1679, Oct. 2008.
• Área do conhecimento: Ciências Biológicas - Imunologia
• Notas: O artigo possui mais de dez autores.
• Citações Web of Science: 45
• Assunto(s): Doenças respiratórias Pulmão Lipopolissacarídeos

Resumo

Background Epidemiological and experimental data suggest that bacterial lipopolysaccharides (LPS) can either protect from or exacerbate allergic asthma. Lipopolysaccharides trigger immune responses through toll-like receptor 4 (TLR4) that in turn activates two major signalling pathways via either MyD88 or TRIF adaptor proteins. The LPS is a pro-Type 1 T helper cells (Th1) adjuvant while aluminium hydroxide (alum) is a strong Type 2 T helper cells (Th2) adjuvant, but the effect of the mixing of both adjuvants on the development of lung allergy has not been investigated. We determined whether natural (LPS) or synthetic (ER-803022) TLR4 agonists adsorbed onto alum adjuvant affect allergen sensitization and development of airway allergic disease. To dissect LPS-induced molecular pathways, we used TLR4-, MyD88-, TRIF-, or IL-12/IFN-GAMMA-deficient mice. Mice were sensitized with subcutaneous injections of ovalbumin (OVA) with or without TLR4 agonists co-adsorbed onto alum and challenged with intranasally with OVA... (AU)

• Processo FAPESP: 05/57136-5 - Modulacao de asma experimental por lipopolissacarideo bacteriano: participacao de tlr4 e myd88, quimiocinas, oxido nitrico e celulas t cd4+.
• Beneficiário: Juliana Bortolatto
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 04/14297-6 - Ativação/desativação de macrófagos e linfócitos T CD4+ na asma experimental
• Beneficiário: Momtchilo Russo
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 06/52705-4 - Tolerancia, tolerancia cruzada e quebra de tolerancia em modelo de asma experimental induzido por blomia tropicalis.
• Beneficiário: Érica Nogueira Borducchi
• Modalidade de apoio: Bolsas no Brasil - Doutorado