Egal E S A, Mariano F V, Blotta M H, Piña A R, Montalli V A, Almeida O P, Altemani A M
Department of Pathology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), São Paulo, Brazil.
Department of Clinical Pathology, Faculty of Medical Sciences, State University of Campinas, São Paulo, Brazil.
Placenta. 2014 Dec;35(12):1021-6. doi: 10.1016/j.placenta.2014.10.004. Epub 2014 Oct 16.
ICAM-1 expression on the villous syncytiotrophoblast (ST) is believed to participate in migration of maternal cells into the inflamed villi regardless of villitis etiology. However, its expression on immune cells in chronic villitis (CV) has yet to be analyzed. ICAM-1 induces cell-cell adhesion allowing intercellular communication, T cell-mediated defense mechanism, and inflammatory response.
21 cases of CV (all without an identifiable etiologic agent) and 3 control placentas were analyzed using ICAM-1, and for immune cells CD45, CD3 and CD68. These cells were subdivided according to their location in inflamed villi: a) within the inflamed villi and b) outside forming perivillous aggregates.
Large amounts of CD45, CD3 and CD68 were found within the inflamed villi and forming perivillous aggregates attached to areas of trophoblastic loss. Inflamed villi usually showed ICAM-1+ ST. The majority of immune cells surrounding areas of trophoblastic rupture presented marked expression of ICAM-1. In contrast, a small number of immune cells within the inflamed villi exhibited ICAM-1 expression. Only some (<5%) inflamed villi without trophoblastic rupture and with ICAM-1+ ST presented adherence of immune cells.
In inflamed villi of chronic villitis, the level of ICAM-1 expression on immune cells depends on their location: high in number of cells in the perivillous region and low within the villi. The strongest expression of ICAM-1 on immune cells attached to areas of trophoblastic rupture suggests that the loss of trophoblast can lead to an amplification of the inflammatory response.
绒毛合体滋养层细胞(ST)上的细胞间黏附分子-1(ICAM-1)表达被认为参与母体细胞向炎症绒毛的迁移,而不考虑绒毛炎的病因。然而,其在慢性绒毛炎(CV)免疫细胞上的表达尚未得到分析。ICAM-1诱导细胞间黏附,促进细胞间通讯、T细胞介导的防御机制和炎症反应。
使用ICAM-1以及免疫细胞标志物CD45、CD3和CD68对21例CV(均无明确病因)和3个对照胎盘进行分析。这些细胞根据其在炎症绒毛中的位置进行细分:a)在炎症绒毛内;b)在绒毛外形成绒毛周围聚集物。
在炎症绒毛内以及形成附着于滋养层缺失区域的绒毛周围聚集物中发现大量CD45、CD3和CD68。炎症绒毛通常显示ICAM-1阳性的ST。滋养层破裂区域周围的大多数免疫细胞呈现ICAM-1明显表达。相比之下,炎症绒毛内少数免疫细胞表现出ICAM-1表达。只有一些(<5%)无滋养层破裂且ICAM-1阳性ST的炎症绒毛出现免疫细胞黏附。
在慢性绒毛炎的炎症绒毛中,免疫细胞上ICAM-1的表达水平取决于其位置:绒毛周围区域细胞数量高,绒毛内低。附着于滋养层破裂区域的免疫细胞上ICAM-1的最强表达表明滋养层的缺失可导致炎症反应的放大。