Possible role of complement factors and their inhibitors in the myocardial infarction: an immunohistochemical study

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.

Keywords: complement inhibitors; complement system; myocardial infarction.

Fig. 1

Complement activation pathways (classical and alternative)

Fig. 2

Morphological assessment of the examined myocardial tissue was done on the basis of the routine hematoxylin and eosin staining. Scale 100 µm

Fig. 3

Immunoreactivity of the complement proteins (C4d and C9) in the examined tissue material. High staining intensity could be seen on the surface of coronary endothelium and moderate staining intensity on single myocardial cells. Scale 50 µm

Fig. 4

Immunoreactivity of membrane complement inhibitors (CD55, CD59) in the tested tissue material. Intensive immunohistochemistry reaction could be seen on the surface of coronary endothelium and weak immunoreactions in sporadic myocardial cells. Scale 50 µm

Fig. 5

Immunoreactivity of membrane complement inhibitors (factor H) in the tested tissue material. Intensive immunohistochemistry reaction could be seen on the surface of coronary endothelium and weak immunoreactions in sporadic myocardial cells. Scale 50 µm