Document Detail


The role of innate immunity in septic acute kidney injuries.
MedLine Citation:
PMID:  20523275     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acute kidney injury (AKI) is an important clinical syndrome characterized by abnormalities in the hydroelectrolytic balance. Because of high rates of morbidity and mortality (from 15% to 60%) associated with AKI, the study of its pathophysiology is critical in searching for clinical targets and therapeutic strategies. Severe sepsis is the major cause of AKI. The host response to sepsis involves an inflammatory response, whereby the pathogen is initially sensed by innate immune receptors (pattern recognition receptors [PRRs]). When it persists, this immune response leads to secretion of proinflammatory products that induce organ dysfunction such as renal failure and consequently increased mortality. Moreover, the injured tissue releases molecules resulting from extracellular matrix degradation or dying cells that function as alarmines, which are recognized by PRR in the absence of pathogens in a second wave of injury. Toll-like receptors (TLRs) and NOD-like receptors (NLRs) are the best characterized PRRs. They are expressed in many cell types and throughout the nephron. Their activation leads to translocation of nuclear factors and synthesis of proinflammatory cytokines and chemokines. TLRs' signaling primes the cells for a robust inflammatory response dependent on NLRs; the interaction of TLRs and NLRs gives rise to the multiprotein complex known as the inflammasome, which in turn activates secretion of mature interleukin 1[beta] and interleukin 18. Experimental data show that innate immune receptors, the inflammasome components, and proinflammatory cytokines play crucial roles not only in sepsis, but also in organ-induced dysfunction, especially in the kidneys. In this review, we discuss the significance of the innate immune receptors in the development of acute renal injury secondary to sepsis.
Authors:
Giselle Martins Gonçalves; Dario S Zamboni; Niels Olsen Saraiva Câmara
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  34 Suppl 1     ISSN:  1540-0514     ISO Abbreviation:  Shock     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-27     Completed Date:  2010-12-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  22-6     Citation Subset:  IM    
Affiliation:
Laboratory of Transplantation Immunobiology, Department of Immunology, Medical School Ribeirão Preto, Universidade de São Paulo, São Paulo, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Acute Kidney Injury / etiology,  immunology*
Animals
Cytokines / physiology
Disease Models, Animal
Humans
Immunity, Innate*
Inflammasomes / physiology
Inflammation
Mice
Nod Signaling Adaptor Proteins / physiology
Receptors, Pattern Recognition / physiology
Renal Circulation
Sepsis / complications,  epidemiology,  immunology*
Toll-Like Receptors / physiology
Chemical
Reg. No./Substance:
0/Cytokines; 0/Inflammasomes; 0/Nod Signaling Adaptor Proteins; 0/Receptors, Pattern Recognition; 0/Toll-Like Receptors

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