Initiation of complement activation following oxidative stress.: In vitro and in vivo observations

Ischemia and reperfusion of organs/tissues induce a state of inflammation that can lead to tissue injury. Focus on development of effective therapeutics based on sound pre-clinical work and the role of leukocytes in models of human disease has not lead to a successful clinical trial for anti-leukocy...

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Bibliographic Details
Published in:Molecular Immunology 2004-06, Vol.41 (2), p.165-171
Main Authors: Hart, Melanie L, Walsh, Mary C, Stahl, Gregory L
Format: Article
Language:English
Subjects:
Animals
Complement Activation - physiology
Complement System Proteins - drug effects
Complement System Proteins - physiology
Gastrointestinal
Humans
Inflammation - etiology
Inflammation - immunology
Inflammation - therapy
Ischemia
Lectin
MBL
Myocardium
Oxidative Stress - immunology
Reperfusion
Reperfusion Injury - immunology
Reperfusion Injury - prevention & control
Reperfusion Injury - therapy
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Summary:Ischemia and reperfusion of organs/tissues induce a state of inflammation that can lead to tissue injury. Focus on development of effective therapeutics based on sound pre-clinical work and the role of leukocytes in models of human disease has not lead to a successful clinical trial for anti-leukocyte technologies. For the past >30 years, it has been known that complement activation plays a role in the inflammation and tissue injury associated with ischemia/reperfusion (I/R) injury. In the last 10 years, several complement inhibitors have made their way from the bench to bedside. Will a complement inhibitor eventually be approved for clinical treatment of I/R type diseases? What pathway(s) are involved in I/R injury, and what role do they play? What specific complement components are needed for resolution of inflammation and what components need to be inhibited to decrease tissue injury? This short review will focus on the current state of the art knowledge about complement, complement pathways, complement components and several promising clinical biologics that inhibit complement activation. This review is not a complete review of complement in ischemia/reperfusion injury, but it raises important questions about the role of complement, its pathways and the current knowledge in the area of ischemia/reperfusion injury.
ISSN:0161-5890
1872-9142
DOI:10.1016/j.molimm.2004.03.013