Document Detail


Leucocyte/endothelium interactions and microvessel permeability: coupled or uncoupled?
MedLine Citation:
PMID:  20472564     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In response to infections or tissue injury, circulating leucocytes adhere to and migrate from the vessel lumen to interstitial inflammatory sites to combat invading pathogens. However, these defensive actions may also cause host tissue injury and microvascular dysfunction through oxidative bursts or enzyme release. For decades, the interaction between leucocytes and microvessel walls has been considered as a critical event leading to organ dysfunction. Extensive investigations have therefore focused on blocking specific adhesive ligands to prevent tissue injury. However, anti-adhesion therapies have shown limited success in preventing vascular dysfunction in clinical trials. Numerous studies have demonstrated temporal and spatial dissociations of leucocyte adhesion and/or emigration from permeability increases. The mechanisms that initiate the adhesion cascade have been found to be distinct from those that trigger the leucocyte oxidative burst responsible for increasing microvessel permeability. Recent studies demonstrated that endothelial activation by inflammatory mediators is critical for initiating platelet adhesion and platelet-dependent leucocyte recruitment resulting in augmented increases in microvessel permeability. These new developments suggest that targeting endothelial activation via directly enhancing endothelial barrier function might be a more efficient strategy than focusing on anti-adhesion or platelet/leucocyte depletion to prevent vascular damage during inflammation. Owing to space limitations and the wide range of studies in the field, this article will not serve as a comprehensive review. Instead, it will highlight the emerging evidence of adhesion-uncoupled permeability changes and establish a basis for re-evaluating the coupled relationship between leucocyte/platelet activation and microvessel permeability to achieve a better understanding of permeability regulation during inflammation.
Authors:
Pingnian He
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2010-05-13
Journal Detail:
Title:  Cardiovascular research     Volume:  87     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-02     Completed Date:  2010-10-12     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  281-90     Citation Subset:  IM    
Affiliation:
Department of Physiology and Pharmacology, School of Medicine, West Virginia University, Morgantown, WV 26506-9229, USA. phe@hsc.wvu.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Platelets / immunology
Body Fluids / metabolism*
Capillary Permeability*
Cell Adhesion
Endothelium, Vascular / immunology,  metabolism*,  physiopathology
Humans
Inflammation / immunology,  metabolism,  physiopathology
Inflammation Mediators / metabolism
Leukocyte Rolling
Leukocytes / immunology*
Microvessels / immunology,  metabolism*,  physiopathology
Neutrophils / immunology
Platelet Adhesiveness
Reactive Oxygen Species / metabolism
Signal Transduction
Grant Support
ID/Acronym/Agency:
HL084338/HL/NHLBI NIH HHS; HL56237/HL/NHLBI NIH HHS; R01 HL056237-13/HL/NHLBI NIH HHS; R01 HL084338-05/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Inflammation Mediators; 0/Reactive Oxygen Species
Comments/Corrections

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


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