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pubmed-article:19501931pubmed:abstractTextAfter treatment with heat-killed Propionibacterium acnes mice show dense hepatic granuloma formation. Such mice develop liver injury in an interleukin (IL)-18-dependent manner after challenge with a sublethal dose LPS. As previously shown, LPS-stimulated Kupffer cells secrete IL-18 depending on caspase-1 and Toll-like receptor (TLR)-4 but independently of its signal adaptor myeloid differentiation factor 88 (MyD88), suggesting importance of another signal adaptor TIR domain-containing adapter inducing IFN-beta (TRIF). Nalp3 inflammasome reportedly controls caspase-1 activation. Here we investigated the roles of MyD88 and TRIF in P. acnes-induced hepatic granuloma formation and LPS-induced caspase-1 activation for IL-18 release.lld:pubmed
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pubmed-article:19501931pubmed:articleTitleContribution of TIR domain-containing adapter inducing IFN-beta-mediated IL-18 release to LPS-induced liver injury in mice.lld:pubmed
pubmed-article:19501931pubmed:affiliationDepartment of Surgery, Hyogo College of Medicine, Nishinomiya, Japan.lld:pubmed
pubmed-article:19501931pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19501931pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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