期刊
NATURE MEDICINE
卷 19, 期 7, 页码 909-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.3221
关键词
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资金
- Instituto Nacional de Ciencia e Tecnologia de Vacinas (INCTV/CNPq)
- Nucleo de Apoio a Pesquisa em Doencas Inflamatorias (NAPDIN) [11.1.21625.01.0]
- Fundacao de Amparo ao Ensino, Pesquisa e Assistencia do Hospital das Clinicas da Faculdade de Medicina de Ribeirao Preto da Universidade de Sao Paulo (FAEPA)
- Special Programme for Research and Training in Tropical Diseases/World Health Organization (TDR/WHO) [A60999]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2006/52867-4, 2009/05054-6]
Parasites of the Leishmania genus are the causative agents of leishmaniasis in humans, a disease that affects more than 12 million people worldwide. These parasites replicate intracellularly in macrophages, and the primary mechanisms underlying host resistance involve the production of nitric oxide (NO). In this study we show that the Nlrp3 inflammasome is activated in response to Leishmania infection and is important for the restriction of parasite replication both in macrophages and in vivo as demonstrated through the infection of inflammasome-deficient mice with Leishmania amazonensis, Leishmania braziliensis and Leishmania infantum chagasi. Inflammasome-driven interleukin-1 beta (IL-1 beta) production facilitated host resistance to infection, as signaling through IL-1 receptor (IL-1R) and MyD88 was necessary and sufficient to trigger inducible nitric oxide synthase (NOS2)-mediated production of NO. In this manuscript we identify a major signaling platform for host resistance to Leishmania spp. infection and describe the molecular mechanisms underlying Leishmania-induced NO production.
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