Mast cells in the placenta. Is there a relation to the development of atopic disease in infants before 18 months of age?

Mikkelsen, Anne Lis; Felding, Christine; Larsen, Lise Grupe; Andersen, Birthe; Sander, Pia

doi:10.1515/jpme.1994.22.4.273

Cited by 4 publications

(2 citation statements)

References 3 publications

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“…An IgE binding capacity in the placenta has been reported previously [34], where mast cells were detected in part by anti‐IgE antibodies. However, the numbers of mast cells in the placenta were not of predictive value for development of atopic disease in children [35]. Our study showed further that mast cell frequency and distribution does not correspond to that of the IgE + cells.…”

Section: Discussioncontrasting

confidence: 48%

IgE is expressed on, but not produced by, fetal cells in the human placenta irrespective of maternal atopy

Sverremark-Ekström

Nilsson

Holmlund

et al. 2002

Clinical and Experimental Immunology

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SUMMARYThe prevalence of atopic diseases in children has increased during the last decades. Atopic symptoms usually appear early in life. This implies an early priming for atopic disease, possibly even at the fetal level. We therefore compared the presence and production of IgE in the local in utero environment during pregnancy in atopic and non-atopic women. Eighty-six women were included in the study. Fifty women were demonstrated to be atopics, based on clinical symptoms of atopic disease together with a positive Phadiatop and/or skin prick test. Placentas from these term pregnancies were obtained. Slices covering the full thickness of the placenta were cut clockwise around the umbilical cord and were analysed with immunohistochemistry. Surprisingly, numerous IgE + cells, located primarily in the fetal villous stroma, were detected in a majority of the investigated placentas irrespective of the atopy of the mother or maternal or fetal total serum IgE levels. The placental IgE could not be demonstrated to be bound to IgE receptors, but was shown to be bound to fetal macrophages, possibly via Fcg RI. No evidence was found for local fetal IgE production, although cells producing epsilon transcripts were occasionally detected in the decidua. We describe here the novel finding of numerous IgE + cells in the human placenta, suggesting an hitherto unknown role for IgE in a successful pregnancy outcome, irrespective of whether or not the mother is atopic.

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Section: Discussioncontrasting

confidence: 48%

IgE is expressed on, but not produced by, fetal cells in the human placenta irrespective of maternal atopy

Sverremark-Ekström

Nilsson

Holmlund

et al. 2002

Clinical and Experimental Immunology

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“…No tryptase-negative subpopulations of mast cells in humans have been found [1,3], although the MC type in human placenta is still unknown [4]. Some investigators have studied correlations between placental MC number and placental pathology during the course of pregnancy and labour [5,6]. Class C diabetes in pregnancy (after White) is the last stage without recognized vascular changes [7].…”

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Placental mast cell heterogeneity in pregnancy complicated by diabetes class C

Szukiewicz¹,

Maślińska

Poppe³

et al. 2000

Inflamm. res.

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IntroductionIn humans, a strict classification into mucosal and connective tissue-type mast cells (MC) is not possible [1]. On the basis of neutral protease composition, human MC have been classified into two phenotypes. One phenotype, which is designated MC T (tryptase-positive, chymase-negative mast cells), contains tryptase but not chymase, while another phenotype, designated MC TC (tryptase-positive, chymase-positive mast cells), expresses both tryptase and chymase [2]. No tryptase-negative subpopulations of mast cells in humans have been found [1,3], although the MC type in human placenta is still unknown [4]. Some investigators have studied correlations between placental MC number and placental pathology during the course of pregnancy and labour [5,6]. Class C diabetes in pregnancy (after White) is the last stage without recognized vascular changes [7]. The results of our recent studies showed, that in diabetes class C an increased density of the villous network of vessels correlates with higher histamine concentrations and increased MC number [6]. Here we examined numbers and distribution of MC T and MC TC in White class C diabetes. Materials and methodsNine placentas obtained from nulliparas after single pregnancies complicated by diabetes White class C (group I; mean gestational age 251 ± 7 days), were compared with nine placentas obtained from gestationally matched preterm controls (group II; mean gestational age 253 ± 5 days). The mean (± SD) fetal/placental weights for group I and group II were: 3431 ± 316 g / 569 ± 51 g, and 3332 ± 321 g / 553 ± 70 g, respectively. The courses of the diabetic pregnancies were normal, without additional medication, except insulin. The control of glycemia in all cases was satisfactory: the levels of fraction of glycosylated hemoglobin (HbA 1c ) in all trimesters of pregnancy were less than 7.5 % (6.3 ± 0.5%).Five placental specimens were obtained immediately after labour in standardised manner, [6]. The samples were fixed in 4 % buffered formalin, embedded in paraffin wax or frozen and cut at 6 mm (5 cuts for each sample). The MC number in placental cuts was estimated after staining with toluidine blue or alcian blue. MC were counted in calibrated areas, using light microscopy with an image analysis system (Quantimet 500C + by Leica). The total number of MC represents the summation of MC numbers from all analysed areas of each placenta. MC protease content was examined using a double-enzyme immunohistochemical staining technique on paraffin sections. Mouse monoclonal antibodies to human MC tryptase and chymase were diluted 1: 2000 -1: 3000 in tris-buffered saline (TBS, pH 7.6) and applied to the tissue sections overnight (12 -14 h) at 4°C. After triple 10 min washing in TBS, biotinylated horse anti-mouse antibody diluted 1: 20 in TBS was applied to the sections for 30 min at room temperature. Sections were washed in TBS and the alkaline phosphatase or peroxidase was developed with appropriate chromogenic substrate at 37°C for 30 min. For each placenta the total number ...

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Placental mast cells (MC) and histamine (HA) in pregnancy complicated by diabetes class C - relation to the development of villous microvessels

Szukiewicz

Maślińska

et al. 1999

Placenta

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Mast cells in the placenta. Is there a relation to the development of atopic disease in infants before 18 months of age?

Abstract: A new predictor, the amount of mast cells in placenta was evaluated. In this study the amount of mast cells, in placenta was not predictive of the development of atopic disease before 18 months of age.

Cited by 4 publications

References 3 publications

IgE is expressed on, but not produced by, fetal cells in the human placenta irrespective of maternal atopy

IgE is expressed on, but not produced by, fetal cells in the human placenta irrespective of maternal atopy

Placental mast cell heterogeneity in pregnancy complicated by diabetes class C

Placental mast cells (MC) and histamine (HA) in pregnancy complicated by diabetes class C - relation to the development of villous microvessels

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