Detection of the terminal complement complex in patient plasma following acute myocardial infarction

Langlois, Paul F.; Gawryl, Maria S.

doi:10.1016/0021-9150(88)90103-7

Cited by 85 publications

(32 citation statements)

References 27 publications

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“…An important pathogenetic role for complement in ischemia/reperfusion of the myocardium was indicated experimentally, where inhibition of the complement cascade greatly reduced myocardial damage after myocardial infarction (109)(110)(111).…”

Section: Ischemia/reperfusion Injuries and Cardiovascular Diseasesmentioning

confidence: 99%

New Insights of an Old Defense System: Structure, Function, and Clinical Relevance of the Complement System

Ehrnthaller

Ignatius

Gebhard

et al. 2010

Mol Med

190

154

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The complement system was discovered a century ago as a potent defense cascade of innate immunity. After its first description, continuous experimental and clinical research was performed, and three canonical pathways of activation were established. Upon activation by traumatic or surgical tissue damage, complement reveals beneficial functions of pathogen and danger defense by sensing and clearing injured cells. However, the latest research efforts have provided a more distinct insight into the complement system and its clinical subsequences. Complement has been shown to play a significant role in the pathogenesis of various inflammatory processes such as sepsis, multiorgan dysfunction, ischemia/reperfusion, cardiovascular diseases and many others. The three well-known activation pathways of the complement system have been challenged by newer findings that demonstrate direct production of central complement effectors (for example, C5a) by serine proteases of the coagulation cascade. In particular, thrombin is capable of producing C5a, which not only plays a decisive role on pathogens and infected/damaged tissues, but also acts systemically. In the case of uncontrolled complement activation, "friendly fire" is generated, resulting in the destruction of healthy host tissue. Therefore, the traditional research that focuses on a mainly positive-acting cascade has now shifted to the negative effects and how tissue damage originated by the activation of the complement can be contained. In a translational approach including structure-function relations of this ancient defense system, this review provides new insights of complement-mediated clinical relevant diseases and the development of complement modulation strategies and current research aspects.

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Section: Ischemia/reperfusion Injuries and Cardiovascular Diseasesmentioning

confidence: 99%

New Insights of an Old Defense System: Structure, Function, and Clinical Relevance of the Complement System

Ehrnthaller

Ignatius

Gebhard

et al. 2010

Mol Med

190

154

View full text Add to dashboard Cite

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“…Since anaphylatoxins are inactivated rapidly (approximately 2 min) [6], determination of their metabolites (C3a desArg, C4a desArg, and C5a desArg) accurately represents the degree of complement activation [9]. Aside from its role in host defense, the complement system has been implicated in the pathophysiology of sepsis [10,11], asthma [12], ischemic/hypoxic injury [13], rheumatoid arthritis [14,15], systematic lupus erythe-matous [16], and delayed type hypersensitivity [17].…”

Section: Introductionmentioning

confidence: 99%

Normal pregnancy is characterized by systemic activation of the complement system

Richani

Soto

Romero

et al. 2005

The Journal of Maternal-Fetal & Neonatal Medicine

177

123

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Background. The complement system, a major component of innate immunity, has recently been implicated in the mechanisms of fetal loss and placental inflammation in the anti-phospholipid antibody syndrome. Inhibition of complement has been proposed as an absolute requirement for normal pregnancy. Yet, pregnancy is characterized by a generalized activation of the innate immune system. This study was conducted to determine whether or not normal pregnancy is associated with complement activation in the maternal circulation. Methods. Anaphylatoxins (C3a, C4a and C5a) were determined in the plasma of normal pregnant (20-42 wks; n = 134) and non-pregnant women (n = 40). These complement split products (C3a, C4a and C5a) were measured using specific immunoassays. Non-parametric statistics were used for analysis. Results. 1) The median plasma concentrations of C3a, C4a and C5a were significantly higher in normal pregnant women than in non-pregnant women (all p 5 0.001); 2) the concentration of C3a, C4a and C5a did not change with gestational age (p 4 0.05); and 3) the median plasma concentration of C3a had a positive correlation with the plasma C4a and C5a concentrations (r = 0.36, p 5 0.001 and r = 0.35, p 5 0.001, respectively). Conclusion. 1) Normal human pregnancy is associated with evidence of complement activation, as determined by higher concentrations of the anaphylatoxins C3a, C4a and C5a in the maternal circulation; and 2) we propose that physiologic activation of the complement system during pregnancy is a compensatory mechanism aimed at protecting the host against infection.

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“…A significant activation of the complement common pathway (from C3 to terminal components) was observed only with SK infusion and is attributable to the rapid formation of immunocomplexes between SK and anti-SK antibodies present in plasma as a consequence of previous streptococcal infections. The AMI,5,6 although two other studies (one, however, was limited to the early phase of AMI) did not report complement activation. 78 We have recently been unable to detect signs of complement activation in plasma during the acute phase of uncomplicated myocardial infarction.…”

mentioning

confidence: 99%

Activation of complement and kinin systems after thrombolytic therapy in patients with acute myocardial infarction. A comparison between streptokinase and recombinant tissue-type plasminogen activator.

et al. 1994

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Background We have previously shown that treatment with streptokinase induces abrupt complement activation and transient neutropenia in patients with acute myocardial infarction (AMI). The purpose of this study was to compare the effects of two different thrombolytic agents -streptokinase (SK) and recombinant tissue-type plasminogen activator (rTPA) -on activation of the complement and kinin systems in plasma of patients with AMI.Methods and Results Forty-one patients with AMI who were eligible for thrombolytic therapy were studied. Twentythree patients were treated with streptokinase (1.5 million IU IV over 60 minutes) and 18 were treated with rTPA (8 with

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Detection of the terminal complement complex in patient plasma following acute myocardial infarction

Cited by 85 publications

References 27 publications

New Insights of an Old Defense System: Structure, Function, and Clinical Relevance of the Complement System

New Insights of an Old Defense System: Structure, Function, and Clinical Relevance of the Complement System

Normal pregnancy is characterized by systemic activation of the complement system

Activation of complement and kinin systems after thrombolytic therapy in patients with acute myocardial infarction. A comparison between streptokinase and recombinant tissue-type plasminogen activator.

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