Elsevier

Placenta

Volume 50, February 2017, Pages 40-43
Placenta

Technical note
Histological changes in the umbilical artery following severe chorioamnionitis and funisitis may be indicative of early atherosclerosis

https://doi.org/10.1016/j.placenta.2016.12.021Get rights and content

Highlights

  • The fetal aorta or umbilical artery may show features of early atherosclerosis.

  • We investigated whether chorioamnionitis with funisitis was pro-atherogenic.

  • CD68 and CD45 positive cells significantly increased in the umbilical artery wall.

  • SMA expression was down regulated in the umbilical artery wall.

  • Chorioamnionitis with funisitis may promote atherogenic changes in fetal vasculature.

Abstract

We investigated whether histological evidence of early atherosclerosis was present in the umbilical artery of 21 pregnancies complicated by severe perinatal inflammation, and 21 controls matched for gestational age, sex and birth weight. Severe chorioamnionitis with funisitis was associated with increased numbers of CD68 and CD45 positive cells (both P < 0.01), indicating accumulation of monocyte-derived macrophages in lesion-susceptible regions. A down-regulation of SMA expression (P = 0.01) was also observed. These preliminary findings suggest that chorioamnionitis with funisitis may promote changes in the intima and media of the umbilical artery similar to that seen in early atherosclerosis.

Introduction

Atherosclerosis is a chronic inflammatory process characterised by immune cell recruitment, lipid accumulation, smooth muscle proliferation and arterial wall thickening [1]. Although the clinical manifestations of atherosclerosis are apparent in adulthood, histological changes indicative of early atherosclerosis, including fatty streaks [2] and intimal thickening [3] may occur in the aorta prior to birth. These features are associated with perinatal cardiovascular risk factors in the mother, including hypercholesterolaemia, diabetes and smoking [4]. Increased umbilical artery intima-media thickness is reported following pregnancies complicated by diabetes [5]. Inflammation is a common mechanism mediating pathogenesis of these maternal risk factors, but there are no data linking perinatal inflammation with early histological changes of atherosclerosis in the umbilical artery. We therefore investigated whether the umbilical arteries from pregnancies complicated by severe chorioamnionitis with funisitis showed histopathologic evidence similar to that seen in early atherosclerosis.

Section snippets

Methods

Paraffin-embedded umbilical cord tissue from pregnancies complicated by severe histological chorioamnionitis with funisitis (n = 21) and controls matched for gestational age (completed weeks), sex and birth weight (±500 g) (n = 21) were identified from recent births at the Royal Women's Hospital (Melbourne, Australia). Severe chorioamnionitis with funisitis was defined by histological evidence of both maternal and fetal inflammatory response ≥ stage 2 by widely used semi-quantitative criteria

Results

Mean birth weight (SD) in cases (3012.91 (675.77) g) was similar to controls (3045.91 (704.19) g; P = 0.88), gestational age (mean 37.24 (3.21) weeks) and sex (43% males) were identical between groups. H&E stained sections from inflamed umbilical arteries showed increased numbers of acute inflammatory cells, with smaller numbers of non-foamy histiocytes and occasional eosinophils, associated with apoptotic debris, and oedema (Fig. 1). Where visible in the plane of section, inflamed umbilical

Discussion

Severe chorioamnionitis with funisitis is associated with significantly increased numbers of non-foamy CD68 and CD45 positive macrophages in the intima and media of the umbilical artery, indicating accumulation of monocyte-derived macrophages in atherosclerosis-prone regions of the arterial wall. These findings are consistent with a vasculitis, however, they are also analogous with the initial cellular changes observed in early (type I) atherosclerotic lesions that precede the development of

Funding sources

This work was supported by the National Health and Medical Research Council (APP1064629), and National Heart Foundation of Australia (100026).

Conflict of interest

The authors declare no conflict of interest.

Acknowledgements

The authors would like to thank Ali Moghimi and Meg Kaegi for their expertise and technical support during the study.

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