Document Detail


Transglutaminase type II is involved in the pathogenesis of endotoxic shock.
MedLine Citation:
PMID:  18250473     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The pathogenesis of sepsis is characterized by the inability of the host to regulate the inflammatory response, and as a consequence, dysregulated inflammatory processes induce organ dysfunctions and death. Altered transglutaminase type II (TG2) expression is associated with the development of many inflammatory diseases. Therefore, in this study, we questioned whether TG2 could also contribute to the pathological inflammatory dysregulation occurring in septic shock in vivo. To this aim, we used as an experimental model the TG2 knockout mice, in which the process of septic shock was elicited by treatment with LPS. Interestingly, our results demonstrated that TG2 ablation leads to partial resistance to experimental sepsis. The increased survival of TG2(-/-) mice was reflected in a drastic reduction of organ injury, highlighted by a limited infiltration of neutrophils in kidney and peritoneum and by a better homeostasis of the proinflammatory mediators as well as mitochondrial function. We also showed that in wild-type mice, the TG2 expression is increased during endotoxemia and, being directly involved in the mechanisms of NF-kappaB activation, it may cause a continuous activation cycle in the inflammatory process, thus contributing to development of sepsis pathogenesis. We propose that the inhibition of TG2 could represent a novel approach in the treatment of inflammatory processes associated with sepsis.
Authors:
Laura Falasca; Maria Grazia Farrace; Alessandra Rinaldi; Loretta Tuosto; Gennard Melino; Mauro Piacentini
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  180     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2008 Feb 
Date Detail:
Created Date:  2008-02-05     Completed Date:  2008-04-17     Revised Date:  2011-11-24    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2616-24     Citation Subset:  AIM; IM    
Affiliation:
Laboratory of Electron Microscopy, National Institute for Infectious Diseases L. Spallanzani, Rome, Italy.
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MeSH Terms
Descriptor/Qualifier:
Acute Kidney Injury / enzymology,  pathology
Animals
Endotoxemia / enzymology,  etiology,  mortality,  pathology
Escherichia coli Infections / enzymology,  mortality,  pathology
Female
GTP-Binding Proteins / biosynthesis,  deficiency,  genetics,  physiology*
Inflammation Mediators / metabolism,  physiology
Lipopolysaccharides / toxicity
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardium / enzymology,  pathology,  ultrastructure
Shock, Septic / enzymology*,  etiology*,  mortality,  pathology
Survival Analysis
Transglutaminases / biosynthesis,  deficiency,  genetics,  physiology*
Grant Support
ID/Acronym/Agency:
GGP06254//Telethon
Chemical
Reg. No./Substance:
0/Inflammation Mediators; 0/Lipopolysaccharides; EC 2.3.2.-/transglutaminase 2; EC 2.3.2.13/Transglutaminases; EC 3.6.1.-/GTP-Binding Proteins

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