Increased Expression of Chemokine Receptor 5 (CCR5) in Blood and Decidual Cells in A Mouse Model for Preeclampsia (PE)

Abstract

A multicascade of leukocyte–endothelial cell interactions is involved in lymphocytes trafficking into tissues. Leukocytes adhesion to the endothelium is mediated by the interaction between endothelial chemokines and their receptors expressed on leukocytes. CCR5 expression has been intensively studied over the last years, since it is not only a trafficking marker, but also a reliable marker to identify Th1 cells. Further, we recently reported a PE mouse model, with increased blood pressure, proteinuria and pathological kidneys accompanied by increased peripheral and local Th1 cytokines levels compared to normal pregnant mice (NP). Here, we investigated whether the extravasation of Th1 lymphocytes into decidua was mediated by CCR5 during experimental PE. We evaluated (1) cytokines secretion and CCR5 expression by immune blood cells and (2) cytokines secretion as well as CCR5 levels in decidual lymphocytes using flow cytometry in PE and NP mice.We observed enhanced production of IL‐12, IFN‐γ and TNF‐α by immune blood cells and augmented number of CCR5+ peripheral cells in PE compared to NP mice. We verified increased production of decidual IL‐12, IFN‐γ and TNF‐α in PE mice. The number of CCR5+ decidual cells was enhanced in PE compared to NP mice.We propose that Th1 lymphocytes migration into decidua is enhanced due to up‐regulated percentages of CCR5+ cells in experimentally induced PE, contributing to the alteration of the physiological parameters observed in this model.