Colloidal carbon blocks oestrogen-induced migration of eosinophils to the uterus and the uterine water imbibition response

Abstract

Oestrogen induces a migration of eosinophil leukocytes to the uterus where, it is suggested, these cells mediate several responses to hormone stimulation. To investigate the mechanism of the recognition of the uterus by the eosinophils, the present study describes the effect of a blockade of the rat reticulo-endothelial system with colloidal carbon on oestrogen-induced uterine eosinophilia, and other responses to oestrogen stimulation that, it has been suggested, are mediated by eosinophils. In the absence of oestrogen colloidal carbon induced an increase in the number of eosinophils in mesometrium but not in endometrium with myometrium, and a slight oedematous reaction in deep endometrium. Colloidal carbon abolished the oestrogen-induced increase in the number of eosinophils in endometrium with myometrium and drastically decreased the oestrogen-induced increase in uterine wet weight and the endometrial oedematous responses 6 h after the administration of oestrogen. The present results agree with the hypothesis that most uterine water imbibition is mediated by eosinophils and suggest a possible mechanism for the interaction of colloidal carbon with eosinophil migration to the uterus.

Genistein Selectively Inhibits Estrogen-Induced Cell Proliferation and Other Responses to Hormone Stimulation in the Prepubertal Rat Uterus

“…The second and third possibilities consider the existence of a different kind of ER that mediates different responses to estrogen stimulation. 7,8,22,[28][29][30][31] Many other explanations may be proposed to explain the selective inhibition of only some responses to estrogen: for instance, subtle differences in ER conformations caused by interaction with different ligands interacting with different co-activators or co-repressors within the cell, 32 and presence of different molecular chaperones (eg FKBP51, FKBP52, and Cyp40), which may be incorporated in the inactivated ER complexes from the different cell types. 33,34 According to our hypothesis, the finding that genistein almost completely inhibited E 2 -induced uterine cell proliferation strongly suggests that genistein is a strong competitive antagonist for ERs involved in these responses.…”