Document Detail


Inflammasome-dependent release of the alarmin HMGB1 in endotoxemia.
MedLine Citation:
PMID:  20802146     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Endotoxin administration recapitulates many of the host responses to sepsis. Inhibitors of the cysteine protease caspase 1 have long been sought as a therapeutic because mice lacking caspase 1 are resistant to LPS-induced endotoxic shock. According to current thinking, caspase 1-mediated shock requires the proinflammatory caspase 1 substrates IL-1β and IL-18. We show, however, that mice lacking both IL-1β and IL-18 are normally susceptible to LPS-induced splenocyte apoptosis and endotoxic shock. This finding indicates the existence of another caspase 1-dependent mediator of endotoxemia. Reduced serum high mobility group box 1 (HMGB1) levels in caspase 1-deficient mice correlated with their resistance to LPS. A critical role for HMGB1 in endotoxemia was confirmed when mice deficient for IL-1β and IL-18 were protected from a lethal dose of LPS by pretreatment with HMGB1-neutralizing Abs. We found that HMGB1 secretion from LPS-primed macrophages required the inflammasome components apoptotic speck protein containing a caspase activation and recruitment domain (ASC), caspase 1 and Nalp3, whereas HMGB1 secretion from macrophages infected in vitro with Salmonella typhimurium was dependent on caspase 1 and Ipaf. Thus, HMGB1 secretion, which is critical for endotoxemia, occurs downstream of inflammasome assembly and caspase 1 activation.
Authors:
Mohamed Lamkanfi; Anasuya Sarkar; Lieselotte Vande Walle; Alberto C Vitari; Amal O Amer; Mark D Wewers; Kevin J Tracey; Thirumala-Devi Kanneganti; Vishva M Dixit
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-08-27
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-22     Completed Date:  2010-10-19     Revised Date:  2012-04-16    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4385-92     Citation Subset:  AIM; IM    
Affiliation:
Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA. Mohamed.Lamkanfi@VIB-UGent.be
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Caspase 1 / immunology,  metabolism
Endotoxemia / immunology,  metabolism*
Enzyme Activation / immunology
Enzyme-Linked Immunosorbent Assay
HMGB1 Protein / immunology,  metabolism*
Inflammation / immunology,  metabolism*
Macrophages / immunology,  metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Microscopy, Fluorescence
Salmonella Infections / immunology,  metabolism
Grant Support
ID/Acronym/Agency:
AR056296/AR/NIAMS NIH HHS; R01 HL076278/HL/NHLBI NIH HHS; R01 HL094586-02/HL/NHLBI NIH HHS; R21 AI083871-01/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/HMGB1 Protein; EC 3.4.22.36/Caspase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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