期刊
JOURNAL OF INFECTIOUS DISEASES
卷 211, 期 2, 页码 322-330出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiu430
关键词
Legionella pneumophila; pulmonary bacterial clearance; neutrophils; MyD88; IL-1 receptor
资金
- Instituto Nacional de Ciencia e Tecnologia em Vacinas
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [2012/09363-6, 2013/08216-2, 2014/04684-4]
- Fundacao de Amparo ao Ensino, Pesquisa e Assistencia do Hospital das Clinicas da Faculdade de Medicina de Ribeirao Preto da Universidade de Sao Paulo
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [12/09363-6, 14/04684-4] Funding Source: FAPESP
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.
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