Document Detail


Oxidized low density lipoprotein and innate immune receptors.
MedLine Citation:
PMID:  14501582     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF REVIEW: Atherosclerosis is now recognized as a chronic inflammatory disease. This review discusses recent literature reporting that innate immune receptors bind oxidatively modified LDL and its many oxidized moieties and consequently modulate the atherogenic process. These innate pattern recognition receptors are known to play a central role in pro-inflammatory responses to bacteria by binding pathogen-associated molecular patterns. It is hypothesized that oxidized LDL exposes similar molecular patterns recognized by receptors of innate immunity. RECENT FINDINGS: Minimally modified LDL and its oxidized phospholipids have been found to bind to CD14 or activate Toll-like receptors on macrophages. In turn, various biological activities have been induced, including the stimulation of cytoskeletal rearrangements that alter phagocytic activity and the stimulation of cytokine secretion, such as IL-8. These findings link modified LDL with innate pattern recognition receptors, such as those involved in the lipopolysaccharide signaling pathway. Human epidemiological studies support the involvement of CD14 and TLR4 in cardiovascular diseases. Oxidized LDL has also been demonstrated to bind to C-reactive protein, an opsonic molecule activating classic complement pathway and Fcgamma receptor endocytosis. These data suggest that C-reactive protein may not only be a strong predictor of clinical disease, but may also play a role in atherogenesis. Recent data on other innate immune receptors are discussed in the context of their potential interactions with oxidized LDL and atherogenesis. SUMMARY: Recent findings suggest that oxidized forms of LDL interact with innate immune receptors. Further studies are needed to identify the role of these interactions in inflammation and atherosclerosis.
Authors:
Yury I Miller; Mi-Kyung Chang; Christoph J Binder; Peter X Shaw; Joseph L Witztum
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Current opinion in lipidology     Volume:  14     ISSN:  0957-9672     ISO Abbreviation:  Curr. Opin. Lipidol.     Publication Date:  2003 Oct 
Date Detail:
Created Date:  2003-09-22     Completed Date:  2004-11-16     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9010000     Medline TA:  Curr Opin Lipidol     Country:  England    
Other Details:
Languages:  eng     Pagination:  437-45     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of California, San Diego, La Jolla, California 92093-0682, USA. yumiller@ucsd.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD14 / metabolism
Arteriosclerosis / metabolism*
C-Reactive Protein / metabolism
Humans
Inflammation / metabolism
Lipoproteins, LDL / metabolism*
Membrane Glycoproteins / metabolism
Receptors, Cell Surface / metabolism
Receptors, Cytokine / metabolism
Receptors, Immunologic / metabolism*
Receptors, Scavenger
Toll-Like Receptor 4
Toll-Like Receptors
Grant Support
ID/Acronym/Agency:
HL56989/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD14; 0/Lipoproteins, LDL; 0/Membrane Glycoproteins; 0/Receptors, Cell Surface; 0/Receptors, Cytokine; 0/Receptors, Immunologic; 0/Receptors, Scavenger; 0/TLR4 protein, human; 0/Toll-Like Receptor 4; 0/Toll-Like Receptors; 0/oxidized low density lipoprotein; 9007-41-4/C-Reactive Protein

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


Previous Document:  New phospholipase A(2) isozymes with a potential role in atherosclerosis.
Next Document:  5-lipoxygenase and atherosclerosis.