Document Detail


SphK1 regulates proinflammatory responses associated with endotoxin and polymicrobial sepsis.
MedLine Citation:
PMID:  20522778     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During sepsis, activation of phagocytes leads to the overproduction of proinflammatory cytokines, causing systemic inflammation. Despite substantial information regarding the underlying molecular mechanisms that lead to sepsis, several elements in the pathway remain to be elucidated. We found that the enzyme sphingosine kinase 1 (SphK1) is up-regulated in stimulated human phagocytes and in peritoneal phagocytes of patients with severe sepsis. Blockade of SphK1 inhibited phagocyte production of endotoxin-induced proinflammatory cytokines. We observed protection against sepsis in mice treated with a specific SphK1 inhibitor that was enhanced by treatment with a broad-spectrum antibiotic. These results demonstrated a critical role for SphK1 in endotoxin signaling and sepsis-induced inflammatory responses and suggest that inhibition of SphK1 is a potential therapy for septic shock.
Authors:
Padmam Puneet; Celestial T Yap; Lingkai Wong; Yulin Lam; Dow Rhoon Koh; Shabbir Moochhala; Josef Pfeilschifter; Andrea Huwiler; Alirio J Melendez
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Science (New York, N.Y.)     Volume:  328     ISSN:  1095-9203     ISO Abbreviation:  Science     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-04     Completed Date:  2010-06-16     Revised Date:  2011-10-24    
Medline Journal Info:
Nlm Unique ID:  0404511     Medline TA:  Science     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1290-4     Citation Subset:  IM    
Affiliation:
Department of Physiology, National University of Singapore, 117597 Singapore.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Aged
Aged, 80 and over
Animals
Bacterial Proteins / immunology
Cytokines / blood,  metabolism*
Endotoxins
Enzyme Activation
Enzyme Inhibitors / pharmacology,  therapeutic use
Female
Humans
Inflammation*
Lipopolysaccharides / immunology
Lipoproteins / immunology
Macrophages / enzymology,  immunology
Macrophages, Peritoneal / enzymology*,  immunology
Male
Mice
Middle Aged
NF-kappa B / metabolism
Neutrophils / enzymology*,  immunology
Peritonitis / enzymology,  immunology
Phosphotransferases (Alcohol Group Acceptor) / antagonists & inhibitors,  genetics,  metabolism*
Protein Kinase C-delta / metabolism
RNA Interference
Sepsis / drug therapy,  enzymology,  immunology*
Shock, Septic / enzymology,  immunology*
Signal Transduction
Up-Regulation
Young Adult
Grant Support
ID/Acronym/Agency:
//Medical Research Council
Chemical
Reg. No./Substance:
0/Bacterial Proteins; 0/Cytokines; 0/Endotoxins; 0/Enzyme Inhibitors; 0/Lipopolysaccharides; 0/Lipoproteins; 0/NF-kappa B; EC 2.7.1.-/Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.-/sphingosine kinase; EC 2.7.11.13/Protein Kinase C-delta
Comments/Corrections
Comment In:
Science. 2011 Oct 21;334(6054):310   [PMID:  22021836 ]
Nat Rev Immunol. 2010 Jul;10(7):464   [PMID:  20589990 ]
Nat Rev Drug Discov. 2010 Jul;9(7):516-7   [PMID:  20592744 ]
Erratum In:
Science. 2011 Jan 14;331(6014):147

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


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