Subject(s)
Adenoma, Pleomorphic/pathology , Carcinoma/pathology , Cell Transformation, Neoplastic , Salivary Gland Neoplasms/pathology , Adenoma, Pleomorphic/epidemiology , Adult , Age Factors , Aged , Carcinoma/epidemiology , Carcinoma in Situ/epidemiology , Carcinoma in Situ/pathology , Humans , Middle Aged , Neoplasm Invasiveness , Retrospective Studies , Risk Factors , Salivary Gland Neoplasms/epidemiology , Tumor BurdenABSTRACT
INTRODUCTION: 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. MATERIAL AND METHODS: 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. RESULTS: 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. DISCUSSION: 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.