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Published on: June 7, 2011
Possible role of complement factors and their inhibitors in the myocardial infarction: an immunohistochemical study
Tomasz Ilczuk1, Aleksander Wasiutynski1, Ewa Wilczek1
1Department of Pathology, Medical University of Warsaw, Warsaw, Poland.
Insights
The complement system, crucial for immunity, contributes to myocardial infarction damage by forming membrane attack complexes on heart cells. Complement inhibitors are also present in damaged heart tissue, suggesting a complex role in heart attack pathogenesis.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Pathophysiology
Background:
- Cardiovascular diseases, particularly myocardial infarction, are a major cause of mortality.
- The precise pathomechanism of myocardial infarction is not fully understood.
- Immune reactions within the myocardium are increasingly recognized as significant factors.
Purpose of the Study:
- To investigate the role of the complement system and its inhibitors in myocardial infarction.
- To examine the presence and localization of complement components and inhibitors in ischemic heart tissue.
Main Methods:
- Immunohistochemistry was used to detect complement components (C4d, C9) and inhibitors (CD55, CD59, factor H).
- Examination of myocardial tissue samples from patients with ischemic necrosis.
Main Results:
- Complement components (C4d, C9) were found to colocalize with complement inhibitors (CD55, CD59, factor H) in ischemic myocardial tissue.
- Positive immunohistochemical reactions were observed in myocardial cells, intercellular matrix, and blood vessels.
Conclusions:
- The complement system is activated in myocardial infarction, leading to the formation of membrane attack complexes that damage heart cells.
- Both complement components and their inhibitors are present in infarcted myocardium, indicating a complex interplay in disease pathogenesis.
Abstract:
Ongoing development of our civilization is accompanied by a marked increase of incidence of cardiovascular diseases and cardiovascular mortality. Ischemic heart disease with its extreme form - myocardial infarction - is one of the main problems of modern medicine. Despite much research devoted to this disease entity, its pathomechanism remains incompletely understood. Basing on research reports, more and more emphasis is put on immune reactions in the myocardium. Available literature lacks detailed studies examining the role of complement system and its inhibitors in the development and pathogenesis of myocardial infarction. Cells of ischemic myocardium were proven to become foreign antigens for the immune system of the patient's body. This results in complement activation of formation of so called membrane attacking complex that injures myocardial cells. By binding to its surface, it extends the myocardial destruction caused by the infarction itself. Results of immunochemistry studies presented in this paper have demonstrated the existence colocalization of complement components (C4d, C9) and membrane inhibitors (CD55, CD59) as well as soluble inhibitors (factor H) of the complement in the examined muscle tissue that underwent ischemic necrosis. Positive immunohistochemical reaction was found in the myocardial cells, intercellular matrix and blood vessels.
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