Apoptosis in placentas from human T-lymphotropic virus type I–seropositive pregnant women: a possible defense mechanism against transmission from mother to fetus

Abstract

Objective: The mechanism by which the placenta serves as the barrier against mother-to-fetus transmission of microorganisms remains to be elucidated. Programmed cell death, apoptosis, is considered a cellular defense mechanism against infection. The hypothesis of this study is that apoptosis of human T-lymphotropic virus type I (HTLV-I)–infected placental villous cells is involved in the defense mechanism against mother-to-fetus transmission of HTLV-I. Methods: Apoptosis was compared in term placentas from eight HTLV-I–seropositive pregnant women and eight HTLV-I–seronegative pregnant women by the terminal deoxynucleotidyl transferase-mediated deoxyuridine nick end-labeling method. In addition, an in vitro cocultivation with an HTLV-I–infected lymphocyte cell line (MT-2 cells) was performed to examine whether placental villous cells were infected with HTLV-I and apoptosis was induced. Results: The incidence of apoptosis-positive cells (nuclei) in placentas from the HTLV-I–seropositive pregnant women was higher than in the HTLV-I–seronegative pregnant women ( P < .02). Cocultivation with MT-2 cells showed that trophoblast cells were able to be infected with HTLV-I and that apoptosis was induced in the placental villous cells. Conclusion: HTLV-I infection induces apoptosis in the placenta. We speculate that apoptosis may be involved in the defense mechanism of the placenta against mother-to-fetus transmission of HTLV-I.