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首页> 外文期刊>Obstetrics and Gynecology: Journal of the American College of Obstetricians and Gynecologists >Apoptosis in placentas from human T-lymphotropic virus type I-seropositive pregnant women: a possible defense mechanism against transmission from mother to fetus.
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Apoptosis in placentas from human T-lymphotropic virus type I-seropositive pregnant women: a possible defense mechanism against transmission from mother to fetus.

机译:人类T型淋巴病毒I型血清反应阳性孕妇胎盘中的细胞凋亡:可能的防御机制,可防止母亲向胎儿传播。

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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.
机译:目的:胎盘作为阻止微生物从母婴传播的屏障的机制尚待阐明。程序性细胞死亡,细胞凋亡被认为是抵抗感染的细胞防御机制。这项研究的假设是,人类T型淋巴病毒I型(HTLV-1)感染的胎盘绒毛细胞的凋亡参与了针对HTLV-1母婴传播的防御机制。方法:采用末端脱氧核苷酸转移酶介导的脱氧尿苷缺口末端标记法,对8例HTLV-1血清阳性孕妇和8例HTLV-1血清阴性孕妇足月胎盘细胞凋亡进行了比较。另外,与HTLV-1感染的淋巴细胞细胞系(MT-2细胞)进行了体外共培养,以检查胎盘绒毛细胞是否被HTLV-1感染并诱导了凋亡。结果:HTLV-I血清阳性孕妇胎盘中凋亡阳性细胞(核)的发生率高于HTLV-1血清阴性孕妇(P <.02)。与MT-2细胞共培养表明滋养层细胞能够被HTLV-1感染,并且胎盘绒毛细胞中诱导了凋亡。结论:HTLV-1感染可引起胎盘凋亡。我们推测凋亡可能参与胎盘对HTLV-1母婴传播的防御机制。

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