Sartelet H, Garraud O, Rogier C, Milko-Sartelet I, Kaboret Y, Michel G, Roussilhon C, Huerre M, Gaillard D
Department of Pathology, Hôpital Principal, Dakar, Senegal.
Histopathology. 2000 Jan;36(1):62-8. doi: 10.1046/j.1365-2559.2000.00742.x.
During pregnancy, Plasmodium falciparum malaria is frequent and associated with maternofetal complications. This could be the consequence of sequestration by several adhesion molecules of parasite-infected red blood cells in syncytiotrophoblast. To investigate the expression of ICAM-1 and CD36, two of the adhesion molecules for Plasmodium falciparum, an immunohistochemical study was carried out in malaria-infected placentas.
Thirty-five infected and 35 noninfected samples were chosen randomly. According to the histological classification of Bulmer, the infected placentas were separated in three groups: active, active chronic and past-chronic infection. CD36 was localized in the cytoplasm of stromal cells of terminal villi of infected or noninfected placentas, but not in syncytiotrophoblast. ICAM-1 was detected in the cytoplasm of stromal and endothelial villous cells in both infected and noninfected placentas and in syncytiotrophoblast of eight infected placentas showing more frequently active than active chronic or past-chronic infection (P < 0.001). The percentage of cells immunostained for CD36 or ICAM-1 was evaluated in the terminal villi. The proportion of villous cells, with ICAM-1 and CD36 immunostaining, was significantly higher in infected vs. noninfected placentas (P < 0.0001) and CD36 was detected more in acute inflammatory vs. past-chronic inflammatory placentas (P < 0.05).
The higher expression of ICAM-1 in infected placentas and its localization in syncytiotrophoblast particularly during acute infection, suggest ICAM-1 can act directly in the sequestration of parasite-infected red blood cells (IRBCs). On the other hand, the expression of CD36 is influenced by the presence of IRBCs without being directly implicated in sequestration of IRBCs. The hyperexpression of these two molecules could explain the high frequency of malaria during pregnancy.
在孕期,恶性疟原虫疟疾较为常见,并与母婴并发症相关。这可能是由于寄生虫感染的红细胞通过几种黏附分子在合体滋养层中滞留所致。为了研究恶性疟原虫的两种黏附分子ICAM - 1和CD36的表达情况,对感染疟疾的胎盘进行了免疫组织化学研究。
随机选取35份感染样本和35份未感染样本。根据布尔默的组织学分类,将感染的胎盘分为三组:活动性、活动慢性和既往慢性感染。CD36定位于感染或未感染胎盘终末绒毛基质细胞的细胞质中,但不在合体滋养层中。在感染和未感染的胎盘的基质和内皮绒毛细胞的细胞质中均检测到ICAM - 1,在8份感染胎盘的合体滋养层中也检测到ICAM - 1,这些胎盘显示活动性感染比活动慢性或既往慢性感染更频繁(P < 0.001)。在终末绒毛中评估CD36或ICAM - 1免疫染色的细胞百分比。与未感染胎盘相比,感染胎盘中有ICAM - 1和CD36免疫染色的绒毛细胞比例显著更高(P < 0.0001),并且在急性炎症胎盘与既往慢性炎症胎盘中检测到的CD36更多(P < 0.05)。
ICAM - 1在感染胎盘中的高表达及其在合体滋养层中的定位,特别是在急性感染期间,表明ICAM - 1可直接作用于寄生虫感染的红细胞(IRBCs)的滞留。另一方面,CDG36的表达受IRBCs存在的影响,但不直接参与IRBCs的滞留。这两种分子的过度表达可能解释了孕期疟疾的高发性。