期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 40, 期 10, 页码 2797-2803出版社
WILEY
DOI: 10.1002/eji.201040490
关键词
Aeromonas; Caspase-1; Nod-like receptor
类别
资金
- Japanese Ministry of Education, Culture, Sports and Technology in Japan [20-08458, 22-3784, 21590484, 21022042]
- Uehara Memorial Foundation
- NOVARTIS Foundation (Japan) for the Promotion of Science
- Grants-in-Aid for Scientific Research [21590484, 21022042] Funding Source: KAKEN
Aeromonas hydrophila is a Gram-negative pathogen that causes serious infectious disease in humans. A. hydrophila induces apoptosis in infected macrophages, but the host proinflammatory responses triggered by macrophage death are largely unknown. Here, we demonstrate that the infection of mouse macrophages with A. hydrophila triggers the activation of caspase-1 and release of IL-1 beta. Caspase-1 activation was abrogated in macrophages deficient in Nod-like receptor family, pyrin domain containing 3 (NLRP3) and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), but not NLR family, CARD domain containing 4 (NLRC4). The activation of the NLRP3 inflammasome was mediated by three cytotoxins (aerolysin, hemolysin and multifunctional repeat-in-toxin) produced by A. hydrophila. Our results indicated that the NLRP3 inflammasome senses A. hydrophila infection through the action of bacterial cytotoxins.
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