期刊
CELL REPORTS
卷 18, 期 5, 页码 1298-1311出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.01.004
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资金
- Japanese Ministry of Education, Culture, Sports, Science and Technology [16H02960]
- Sumitomo Science Foundation
- Platform Project for Supporting in Drug Discovery and Life Science Research from Japan Agency for Medical Research and Development (AMED)
- Naito Research Foundation
- Grants-in-Aid for Scientific Research [16K15112, 16H02960, 15KK0327] Funding Source: KAKEN
The inhalation of silica dust is associated with fibrosis and lung cancer, which are triggered by macrophage inflammatory responses; however, how macrophages recognize silica remains largely unknown. Here, we identify by functional expression cloning the class B scavenger receptor SR-B1 as a silica receptor. Through an extracellular alpha-helix, both mouse and human SR-B1 specifically recognized amorphous and crystalline silica, but not titanium dioxide nanoparticles, latex nanoparticles, or monosodium urate crystals, although all particles exhibited negative surface potentials. Genetic deletion of SR-B1 and masking of SR-B1 by monoclonal antibodies showed that SR-B1-mediated recognition of silica is associated with caspase-1-mediated inflammatory responses in mouse macrophages and human peripheral blood monocytes. Furthermore, SR-B1 was involved in silica-induced pulmonary inflammation in mice. These results indicate that SR-B1 is a silica receptor associated with canonical inflammasome activation.
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