Thushari I Alahakoon1,2, Heather Medbury1,3, Helen Williams1,3, Nicole Fewings1,4, Xin M Wang1,5, Vincent W Lee1,6. 1. Westmead Clinical School, University of Sydney, Sydney, New South Wales, Australia. 2. Westmead Institute for Maternal and Fetal Medicine, Westmead Hospital, Westmead, New South Wales, Australia. 3. Department of Surgery, Westmead Hospital, Westmead, New South Wales, Australia. 4. Department of Immunology, Westmead Hospital, Westmead, New South Wales, Australia. 5. Flow Cytometry Core Facility, Westmead Research Hub, Westmead, New South Wales, Australia. 6. Department of Renal Medicine, Westmead Hospital, Westmead, New South Wales, Australia.
Abstract
AIM: Monocytes are likely to play a significant role in the pathogenesis of preeclampsia (PE) and intrauterine fetal growth restriction (IUGR), given their role in homeostasis and tissue repair. Our aim was to study the gestational changes in monocytes in normal pregnancy and to determine whether monocyte subsets and phenotype are altered in pregnancy complications, such as PE and IUGR. METHODS: A prospective cross-sectional case-control study was conducted. Pregnant women between 24 and 40 weeks of gestation (n = 54) were recruited and classified into four clinical groups of normal pregnancy, PE, IUGR and PE + IUGR. The maternal monocyte subsets classical, intermediate and nonclassical were compared for each clinical group. Monocyte polarization towards M1 (inflammatory) and M2 (repair) phenotypes was assessed by surface expression of CD86 and CD163 ratio, using flow cytometry. RESULTS: The classical monocytes were reduced and intermediate monocyte elevated compared to normal pregnancy in PE, IUGR and PE + IUGR in gestations <37 weeks and IUGR in 26-40 weeks. CD163 expression was increased and CD86/CD163 ratio decreased in IUGR compared to normal pregnancy for all subsets. Nonclassical monocyte counts and CD163 expression increased with advancing gestation in normal pregnancy. CONCLUSION: These results show for the first time, a shift towards increased intermediate maternal monocyte subtype in IUGR and in preterm PE as well as skewing of maternal peripheral monocytes (all subsets) towards M2 phenotype in pregnancies complicated by IUGR.
AIM: Monocytes are likely to play a significant role in the pathogenesis of preeclampsia (PE) and intrauterine fetal growth restriction (IUGR), given their role in homeostasis and tissue repair. Our aim was to study the gestational changes in monocytes in normal pregnancy and to determine whether monocyte subsets and phenotype are altered in pregnancy complications, such as PE and IUGR. METHODS: A prospective cross-sectional case-control study was conducted. Pregnant women between 24 and 40 weeks of gestation (n = 54) were recruited and classified into four clinical groups of normal pregnancy, PE, IUGR and PE + IUGR. The maternal monocyte subsets classical, intermediate and nonclassical were compared for each clinical group. Monocyte polarization towards M1 (inflammatory) and M2 (repair) phenotypes was assessed by surface expression of CD86 and CD163 ratio, using flow cytometry. RESULTS: The classical monocytes were reduced and intermediate monocyte elevated compared to normal pregnancy in PE, IUGR and PE + IUGR in gestations <37 weeks and IUGR in 26-40 weeks. CD163 expression was increased and CD86/CD163 ratio decreased in IUGR compared to normal pregnancy for all subsets. Nonclassical monocyte counts and CD163 expression increased with advancing gestation in normal pregnancy. CONCLUSION: These results show for the first time, a shift towards increased intermediate maternal monocyte subtype in IUGR and in preterm PE as well as skewing of maternal peripheral monocytes (all subsets) towards M2 phenotype in pregnancies complicated by IUGR.