Atherosclerotic plaques exhibit a series of features that are similar to those of chronic
inflammation. Based on the fact that during
inflammation several cell types synthesize and secrete a group II
phospholipase A2 (PLA2), an immunohistochemical study was undertaken to explore whether this
enzyme can be identified in human atherosclerotic lesions. Tissue specimens obtained from 13 patients who had undergone arteriectomy and three specimens with advanced
atherosclerotic plaques obtained at autopsy were analyzed and compared to arteries free of
atherosclerosis. The results showed that in all areas with atherosclerotic lesions, a staining with
monoclonal antibodies raised against group II PLA2 was evident. In normal arteries without thickened intima, this immunostaining was completely negative. With the use of specific
monoclonal antibodies against macrophages (anti-KP-1) and smooth muscle cells (anti-
alpha-actin), PLA2-positive cells were identified as foam cells mainly derived from macrophages. In addition to these cells, other regions of the thickened intima gave a partially positive reaction with anti-PLA2
antibodies, but could not be stained with either anti-KP-1 or anti-
alpha-actin. Some of these regions were localized on edges of calcification and cell
necrosis. Other PLA2-positive regions seem to be associated with extracellular matrix structures. In summary, the findings of this study may be regarded as further evidence to support the link between
atherosclerosis and chronic inflammatory processes. In view of the fact that the in vitro modification of
lipoproteins by PLA2-treatment induces
lipid deposition in macrophages, the results of this study suggest that group II PLA2 may actively be involved in the formation of foam cells in vivo.