"Acute atherosis" is characteristic in the spiral arteries of the placental bed of preeclampsia and a wide range of pregnancy disorders. The arterial lesion is histologically characterized by fibrinoid necrosis of the vessel walls with infiltration of foam cells, which under a light microscope appears similar to that seen in atherosclerosis. Although acute atherosis is currently considered as atheromatous-like lesions, the precise cellular mechanisms inducing these changes remain unelucidated. By histochemistry, immunohistochemistry, and electron microscopy, we investigated the decidual spiral arteries obtained by placental bed biopsy from 11 preeclamptic and 15 nonpreeclamptic women. In the decidual spiral arteries of preeclamptic patients, acute atherosis was observed in 23.5% (20/85 arteries). Fibrin deposition and accumulation of foam cells were observed more frequently in preeclamptic patients than in nonpreeclamptic patients. Endothelial cells remained in the atheromatous lesion, while the smooth muscle layer surrounding fibrin and foam cells became thin and was finally destroyed. The foam cells were immunohistochemically shown to be macrophages and neutral fat and phospholipids were histochemically demonstrated in them. Ultrastructurally, their cytoplasm was occupied by variously sized lipid droplets and membrane-bound myelin-like granules (myelinosomes). Plasma concentration of monocyte chemoattractant protein 1 (MCP-1), a potent monocyte chemoattractant factor, was significantly elevated in preeclamptic patients compared with normal healthy controls (P < 0.01). In conclusion, injuries to the smooth muscle layer and intramural fibrinoid necrosis may result in infiltration of monocytes into the arterial walls, their maturation into macrophages, and the transformation into foam cells. Considering that atherosclerosis is developed by accumulation of lipid-laden macrophages and migration and proliferation of smooth muscle cells, the roles of macrophages in acute atherosis differ from those in atherosclerosis.

It is well known that the number of peritoneal macrophages is increased in patients with pelvic endometriosis. We measured the concentration of monocyte chemoattractant protein-1 (MCP-1) using an enzyme-linked immunosorbent assay (ELISA) in the peritoneal fluid of women with and without endometriosis. The expression of MCP-1 in pelvic endometriotic lesions obtained from the peritoneum was also examined using immunohistochemistry and nonradioactive in situ hybridization. The mean concentration of MCP-1 in the peritoneal fluid was significantly higher in the patients with endometriosis (P<0.05). The most significant elevation, compared with non-endometriosis patients, was found in stage I of the disease (P<0.05). However, no statistically significant difference was found among endometriosis stages I, II, III, and IV. Immunohistochemical staining revealed that MCP-1-positive cells were localized in the glandular epithelium of the endometriotic lesions and in the stromal macrophages distributed in those lesions, but normal peritoneal cells were negative. The in situ hybridization method demonstrated expression of MCP-1 mRNA on the endometriotic glandular epithelium and stromal macrophages. These findings suggest that MCP-1 may be involved in the histogenesis and early development of peritoneal endometriosis.