Interleukin 1 Receptor-Driven Neutrophil Recruitment Accounts to MyD88-Dependent Pulmonary Clearance of Legionella pneumophila Infection In Vivo

Autor(es)

Mascarenhas, Danielle P. A. ^[1] ; Pereira, Marcelo S. F. ^[1] ; Manin, Graziele Z. ^[1] ; Hori, Juliana I. ^[1] ; Zamboni, Dario S. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Cell Biol, BR-05508 Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Journal of Infectious Diseases; v. 211, n. 2, p. 322-330, JAN 15 2015.
• Citações Web of Science: 15

Resumo

Legionella pneumophila, the etiological agent of Legionnaires' disease, triggers activation of multiple innate immune pathways that lead to the restriction of bacterial replication in vivo. Despite the critical role for MyD88 in infection clearance, the receptors and mechanisms responsible for MyD88-mediated pulmonary bacterial clearance are still unclear. Here, we used flagellin mutants of L. pneumophila, which bypass the NAIP5/NLRC4-mediated restriction of bacterial replication, to assess the receptors involved in MyD88-mediated pulmonary bacterial clearance. By systematically comparing pulmonary clearance of L. pneumophila in C57BL/6 MyD88(-/-), TLR2(-/-), TLR3(-/-), TLR4(-/-), TLR9(-/-), IL-1R(-/-), and IL-18(-/-) mice, we found that, while the knockout of a single Toll-like receptor or interleukin 18 resulted only in minor impairment of bacterial clearance, deficiency in the interleukin 1 (IL-1) receptor led to a significant impairment. IL-1/MyD88-mediated pulmonary bacterial clearance occurs via processes involving the recruitment of neutrophils. Collectively, our data contribute to the understanding of the effector mechanisms involved in MyD88-mediated pulmonary bacterial clearance. (AU)

• Processo FAPESP: 12/09363-6 - Patogênese molecular e subversão das respostas do hospedeiro em infecções por Legionella spp.
• Beneficiário: Dario Simões Zamboni
• Linha de fomento: Auxílio à Pesquisa - Regular
• Processo FAPESP: 14/04684-4 - O inflamassoma na resposta contra patógenos intracelulares e os mecanismos microbianos relacionados à evasão
• Beneficiário: Dario Simões Zamboni
• Linha de fomento: Auxílio à Pesquisa - Temático
• Processo FAPESP: 13/08216-2 - CPDI - Centro de Pesquisa em Doenças Inflamatórias
• Beneficiário: Fernando de Queiroz Cunha
• Linha de fomento: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs