CCR3 antagonist impairs estradiol-induced eosinophil migration to the uterus in ovariectomized mice.

J.M.D Araújo,R Grespan,L.A.S Silva,F.B Felix,E.A Camargo

doi:10.1590/1414-431x20198659

J.M.D Araújo, R Grespan + Show 3 more

Open Access

https://doi.org/10.1590/1414-431x20198659

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Abstract

Eosinophils are abundant in the reproductive tract, contributing to the remodeling and successful implantation of the embryo. However, the mechanisms by which eosinophils migrate into the uterus and their relationship to edema are still not entirely clear, since there are a variety of chemotactic factors that can cause migration of these cells. Therefore, to evaluate the role of CCR3 in eosinophil migration, ovariectomized C57BL/6 mice were treated with CCR3 antagonist SB 328437 and 17β-estradiol. The hypothesis that the CCR3 receptor plays an important role in eosinophil migration to the mouse uterus was confirmed, because we observed reduction in eosinophil peroxidase activity in these antagonist-treated uteruses. The antagonist also influenced uterine hypertrophy, inhibiting edema formation. Finally, histological analysis of the orcein-stained uteruses showed that the antagonist reduced eosinophil migration together with edema. These data showed that the CCR3 receptor is an important target for studies that seek to clarify the functions of these cells in uterine physiology.

Highlights

The participation of eosinophils in the female reproductive tract has been reported since the 1960s [1]
Analysis of the uterus wet weight demonstrated that after 24 h, the E2-injected animals (100 mg/kg) presented significant uterine edema, causing an increase of 40% in uterus weight compared with the group that received only sesame oil (SO) (Figure 1A)
Different doses of E2 (0.1, 1, 10, and 100 mg/kg) were tested and doses of 1, 10, and 100 mg/kg were effective in inducing uterine edema 24 h after E2 administration

Summary

Introduction

The participation of eosinophils in the female reproductive tract has been reported since the 1960s [1]. The first studies observed eosinophil migration to the uterus elicited by estrogen but not progesterone [2]. In immature rats, this migration has been accompanied by uterine edema [3]. Estrogen circulation promotes the increase in uterine eosinophils, and these cells are linked to tissue remodeling and maintenance of the normal estrous cycle in rodents [4,5]. Eosinophils present in the endometrium during genital pathogen infection secrete IL-4 to promote vascular stromal cell proliferation and repair of injured endometrial tissue [7]

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