Role of eosinophils in uterine responses to estrogen

• Published in: Biology of reproduction Vol. 54; no. 1; pp. 249 - 254
• Main Authors: PEREZ, M. C, FURTH, E. E, MATZUMURA, P. D, LYTTLE, C. R
• Format: Journal Article
• Language: English
• Published: Madison, WI Society for the Study of Reproduction 01.01.1996
• Subjects: Animals; Antibodies, Monoclonal - pharmacology; Biological and medical sciences; Chemotaxis, Leukocyte - drug effects; Eosinophils - physiology; Estradiol - pharmacology; Female; Fundamental and applied biological sciences. Psychology; Immunoglobulin G - pharmacology; Interleukin-5 - immunology; Interleukin-5 - physiology; Leukocyte Count; Mammalian female genital system; Mice; Mice, Inbred BALB C; Morphology. Physiology; Ovariectomy; Peroxidase - metabolism; Uterus - cytology; Uterus - drug effects; Uterus - growth & development; Vertebrates: reproduction; Ovariectomy; Estrogen; Rodentia; 17β-Estradiol; Ovarian hormone; Eosinophil; Chemotactic factor; In vivo; Vertebrata; Mammalia; Mouse; Uterus; Female genital system; Hormonal regulation; Development; Female
• ISSN: 0006-3363; 1529-7268
• DOI: 10.1095/biolreprod54.1.249

Administration of estradiol (E2) to ovariectomized mice results in a dramatic increase in uterine growth and an influx of eosinophilic leukocytes. This influx is mediated by stimulation of an E2-dependent eosinophilic chemotactic factor in the uterus (ECF-U). The role of this eosinophil infiltration in uterus is presently unknown but could involve early growth and/or remodeling processes. In an attempt to better define eosinophil function in uterine tissue, we produced ovariectomized mice severely depleted of circulating eosinophils by administration of a purified rat IgG monoclonal antibody against interleukin-5 (IL-5). Seven days later, animals were submitted to estradiol treatment. Experimental groups included mice treated with saline alone, saline followed by E2, IgG followed by E2, and anti-IL-5 followed by E2. Pretreatment with IL-5 antibodies led to no significant alteration in E2-induced increase in uterine wet weight. However, histological evaluation demonstrated a clear and almost complete blockade of E2-stimulated influx of eosinophils in anti-IL-5 treated animals. In addition, IL-5 antibody administration significantly reduced E2-induced increase in peroxidase activity. Dramatic reduction of eosinophils did not affect E2 stimulation of ECF-U activity by stromal cells or complement C3 synthesis by the epithelial cells. Thus, it appears that differences in E2 responses in eosinophil-deficient mice are not directly associated with presence or absence of eosinophils. Taken together, these data suggest that eosinophils most likely do not contribute to early growth in the E2-stimulated uterus. A possible role in other events such as remodeling remains to be elucidated.