Characterization of macrophages in the decidual atherotic spiral artery with special reference to the cytology of foam cells

Abstract

"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.

Chitotriosidase, interleukin-1 beta and tumor necrosis factor alpha levels in mild preeclampsia

“…Aberrant decidual macrophage distribution and function have been described in patients with preeclampsia [4,7,8]. Immunohistochemical analysis of placental bed biopsies has demonstrated an accumulation of macrophages surrounding acute atherosis lesions within the spiral arteries in preeclamptic patients [20]. The infiltrating macrophages could affect trophoblast function in various ways: induce apoptosis [21], alter differentiation or proliferation [22] and may also hamper trophoblast invasion [6].…”

Oxidative stress markers in severe preeclampsia and preeclampsia-related perinatal morbidity — preliminary report

“…The characteristic vascular lesions in preeclampsia were shown to be similar to atherosclerotic plaques with lipid accumulation and infiltration of foam cells. Thus, it has been proposed that the changes in preeclampsia may be mediated by abnormal lipid peroxidation [13,14]. Lipid peroxidation causes cellular damage and vascular endothelial cell injury, and is used as an indicator of oxidative stress [15].…”

Spiral artery remodeling and maternal cardiovascular risk

“…Apart from abnormal spiral artery remodeling, women with preeclampsia also show other characteristic placental vascular abnormalities described as 'acute atherosis' [12][13][14]. These lesions are more likely to occur in the decidual part of the placental bed and in vessels of the membranes, and are accompanied by inflammation and several features similar to vascular pathology found in early-stage atherosclerosis, including lipid accumulation in macrophages (foam cells) [15,16].…”