Abstracts

Abstract

Fetal cells enter the maternal circulation during all human and murine pregnancy. The presence of fetal microchimeric cells has been demonstrated in lesional skin of pregnant women affected with polymorphic eruptions of pregnancy. We aimed at determining in a mouse model the role of maternal inflammation in attracting microchimeric cells. Wild type female mice were mated to transgenic males for various reporter genes or wild type male controls. We used males transgenic for the luciferase gene under the control of an ubiquitous (CMV)(C-Luc) or the VEGFR2 (V-Luc) promoter. Alternatively we used males transgenic for the EGFP under the control of the beta-actin promoter. Female pregnant mice were sensitized on day 10 of pregnancy with 2% Oxazolone. On day 16 we revealed a contact hypersensitivity reaction (CHR) by painting the right ear with oxazolone while the left ear received only the vehicle. The presence of fetal cells was then monitored using one of the following: in vivo imaging to detect luciferase expressing fetal cell real time quantitative amplification of the egfp transgene or Y chromosome in situ hybridization to detect male microchimeric cells. On femalemice bearing V-Luc fetuses, a fetal signal could be detected only on the right ear that was significantly higher when compared to controls (3362 versus 1507 photons/s/cm2, p=0.02). Wealso detected fetal cells by real time quantitative PCR in the right as well as the left ear at similar frequencies. Finally, we demonstrated the presence of fetal cells in maternal inflamed ears. Fetal cells were either among the inflammatory cells or were part of the vascular wall. We demonstrate that maternal inflamed skin can recruit fetal microchimeric cells. The fetal cells adopt an endothelial phenotype in the inflamed maternal skin. Fetal cells may therefore participate in maternal angiogenesis and inflammation.