PubMed · 3724062
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E Angel, J R Davis, R B Nagle. 1986. Decidual cells.. https://pubmed.ncbi.nlm.nih.gov/3724062/
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OBJECTIVE: To distinguish endocrine and paracrine influences on leukocyte subpopulations at uterine and tubal implantation sites. DESIGN: Retrospective immunohistochemical study. SETTING: Departments of Anatomy, and Obstetrics and Gynecology, School of Medicine, RWTH University of Aachen, Aachen, Germany. PATIENT(S): Ten women with a viable ectopic pregnancy (EP), 25 women who had undergone elective first-trimester termination of pregnancy, and 4 women who had undergone hysterectomy with adnexectomy. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Quantitative analysis of leukocyte subpopulations at the implantation sites and their corresponding noninvaded tissues, decidual tissue from patients with EP, and tubal mucosa from normal menstrual cycle. RESULT(S): Similar numbers and characteristic distribution patterns of macrophages, T cells, and B cells were found at both normal intrauterine and tubal implantation sites. Natural killer (NK) cells were always absent from tubal mucosa. The number and distribution of leukocytes within decidual tissue from women with EP corresponded to those in the noninvaded decidual compartment in intrauterine pregnancy (IUP). CONCLUSION(S): Leukocyte populations present in the tubal and uterine mucosa are an intrinsic characteristic of these tissues. The distinct leukocyte distribution pattern at the implantation sites suggests that the invading trophoblast exerts a paracrine influence on endometrial and endosalpingeal leukocytes. The absence of natural killer cells from the tubal wall may be one reason for the higher degree of invasiveness of the trophoblast at the tubal implantation site.
The intrauterine environment is characterized by a Th2 dominance during pregnancy, a milieu that also promotes atopic allergy. The aim of this study was to compare the presence of CD30, a molecule associated with Th2 related disorders such as atopic allergy, and its ligand (CD30L) in placenta in order to investigate if the placenta environment differs between atopic and non-atopic women. Serum concentrations of soluble CD30 (sCD30) from the mothers and their newborns were also elucidated. There were no differences in the immunohistochemical expression of CD30 and CD30L in placenta from atopic (n=28) compared with non-atopic (n=37) women. CD30 was expressed on the decidual stromal cells alone, while CD30L, previously not described in placenta, was detected on macrophage-like HLA-DR(+) cells throughout the mesenchymal chorionic villi. Serum sCD30 in atopic mothers was significantly elevated compared with serum sCD30 in non-atopic mothers (P< 0.05), while sCD30 levels in cord blood were similar in both groups independently of maternal atopic heredity. We suggest that sCD30 in cord blood and CD30 expression by decidual cells may reflect the Th2 environment surrounding the fetus, and both CD30 and CD30L could have immune regulatory functions in placenta.
BACKGROUND: Preeclampsia is a progressive, multisystem disorder characterised by hypertension and proteinuria. A body of evidence suggest a genetic basis; it is generally accepted that the underlying pathological processes are in the placenta. MATERIAL AND METHODS: This article is a review of the pathophysiology of preeclampsia based on literature mainly obtained through PubMed and Medline searches. RESULTS: A poorly perfused placenta, secondary to defective placental invasion of the spiral arteries, may lead to hypoxia and insufficient perfusion and cause release of cytokines which damage endothelial cells and cause dysfunction. Women with preeclampsia have markedly elevated concentrations of triglyceride-rich lipoproteins. Lipid peroxidation also causes endothelial dysfunction and thus contributes to preeclampsia. Placenta is one source of the lipid peroxides. Antioxidant deficiency is also a predisposing factor. Hyperhomocysteinaemia, protein S and protein C deficiency, and activated protein C resistance appear to be involved in the pathophysiology of severe preeclampsia and early onset preeclampsia. INTERPRETATION: The new information about mechanisms for development of preeclampsia gives a basis for new treatment modalities.