Section of Parasitology, Department of Zoology, Aligarh Muslim University, Aligarh, 202002, India.
Section of Parasitology, Department of Zoology, Aligarh Muslim University, Aligarh, 202002, India.
Placenta. 2022 Sep;127:52-61. doi: 10.1016/j.placenta.2022.07.017. Epub 2022 Aug 9.
Pregnant women are more susceptible to malaria due to a combination of physiological and immunological changes. The infection may even affect the growth and survival of the foetus, which mainly occur when parasite enters the placenta. The sequestration of infected erythrocytes may trigger the host response, leading to placental inflammation and altered development, affecting the structure and nutrient transport of placenta. These factors collectively impair placental functions and affect foetal growth.
Pregnant women with peripheral parasitaemia for P. falciparum and P. vivax (20 each) were included in the present study, along with 15 age-matched uninfected healthy pregnant women. Placentae were analysed for the presence of local parasitaemia along with pathological lesions caused due to the parasite. Immunohistochemical staining for CD20, CD45 and CD68 cells was performed for examining the specific leucocytes in the intervillous space of the placenta.
Of the 20 individuals with P. falciparum, only seven placentae showed parasitaemia, whereas individuals with P. vivax showed no placental infection. The pathological changes observed in the P. falciparum-infected placenta include syncytial knotting, excess fibrinoid deposition, syncytiotrophoblast necrosis, syncytial rupture, thickening of trophoblast basement membrane and increased collagen deposition. Immunohistochemical staining showed a significant increase in B cells (CD20), leucocytes (CD45) and monocytes and macrophages (CD68) in the P. falciparum-infected placenta (p < 0.0001).
The result implies that P. falciparum is responsible for pathological alterations in placenta, affecting the nutrient transport across placenta and foetal growth. The immune cells also migrate to the placenta and accumulate in the intervillous space to show humoral and cell-mediated immunity against the parasite.
由于生理和免疫变化的综合作用，孕妇更容易感染疟疾。寄生虫进入胎盘时，感染甚至可能影响胎儿的生长和存活。受感染的红细胞的隔离可能会引发宿主反应，导致胎盘炎症和发育改变，影响胎盘的结构和营养物质转运。这些因素共同损害胎盘功能并影响胎儿生长。
本研究纳入了外周有恶性疟原虫和间日疟原虫寄生的孕妇（各 20 例），以及 15 例年龄匹配的未感染的健康孕妇。分析胎盘是否存在局部寄生虫血症以及寄生虫引起的病理损伤。通过 CD20、CD45 和 CD68 细胞的免疫组织化学染色，检查胎盘绒毛间隙中的特定白细胞。
在 20 例恶性疟原虫感染者中，只有 7 例胎盘有寄生虫血症，而间日疟原虫感染者的胎盘无感染。在恶性疟原虫感染的胎盘组织中观察到的病理变化包括合体滋养层结节、纤维蛋白样物质沉积过多、合体滋养层细胞坏死、合体滋养层破裂、滋养层基膜增厚和胶原沉积增加。免疫组织化学染色显示，恶性疟原虫感染的胎盘内 B 细胞（CD20）、白细胞（CD45）和单核细胞/巨噬细胞（CD68）明显增加（p<0.0001）。
结果表明恶性疟原虫是导致胎盘病理改变的原因，影响了营养物质穿过胎盘的转运和胎儿生长。免疫细胞也迁移到胎盘并在绒毛间隙内聚集，以针对寄生虫产生体液和细胞免疫。
