title: Immunohistochemical characterization of the estrogen-stimulated leukocyte influx in the immature rat uterus.
abstract: Previous studies have shown that the injection of estrogen into immature rats leads to an influx of leukocytes into the uterus. Using immunoperoxidase staining and monoclonal antibodies, we have characterized the nature of the infiltrating leukocytes in frozen sections of immature rat uteri obtained following the injection of estrogen, estrogen plus pertussigen, and the antiestrogen LY117018. Estradiol treatment for 2 days resulted in a significant increase in the number of uterine eosinophils, CD4 (W3/W25)-positive helper/inducer T lymphocytes, macrophages (MRC OX-42-positive cells), and Ia (MRC OX-6)-positive cells. In contrast, estradiol treatment failed to elicit a significant increase in the number of CD8 (MRC OX-8)-positive uterine cytotoxic/suppressor T lymphocytes and/or natural killer cells, as well as MAR 18.5- and/or MRC OX-12-positive B lymphocytes. The injection of LY117018 failed to elicit any changes in the number of cells expressing any of the phenotypes under investigation. The simultaneous injection of pertussigen, the major toxin responsible for the leukocytosis- and lymphocytosis-promoting activity of Bordetella pertussis, inhibited the estrogen-induced influx of eosinophils, macrophages (MRC OX-42-positive cells), and Ia (MRC OX-6)-positive cells but failed to prevent the influx of CD4 (W3/25) positive helper/inducer T lymphocytes. These results indicate that, in the immature rat, significant differences may exist in the susceptibility of various cell populations to the effects of estrogen, particularly with regard to uterine influx following estrogen stimulation. In addition, our observations suggest that either 1) the CD4-positive cells infiltrating the uterus following estrogen treatment may use a nonpertussigen-sensitive mechanism for chemotactic factor-receptor signal transduction or 2) a subpopulation of resident uterine cells can be induced to express the CD4 antigen following estrogen and/or estrogen plus pertussigen treatment.
authors.affiliation: Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia 19104-6080.
authors.forename: Y
authors.initials: Y
authors.lastname: Zheng
authors.forename: Z Z
authors.initials: ZZ
authors.lastname: Zhou
authors.forename: C R
authors.initials: CR
authors.lastname: Lyttle
authors.forename: C
authors.initials: C
authors.lastname: Teuscher
mesh_terms: D000818:Animals; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D002465:Cell Movement / Q000187:drug effects; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D007150:Immunohistochemistry; D007962:Leukocytes / Q000187:drug effects* / Q000502:physiology; D037342:Pertussis Toxin; D011759:Pyrrolidines / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013876:Thiophenes / Q000494:pharmacology; D014599:Uterus / Q000166:cytology / Q000187:drug effects*; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D004967:Estrogens; D000949:Histocompatibility Antigens Class II; D011759:Pyrrolidines; D013876:Thiophenes; D010566:Virulence Factors, Bordetella; C025430:LY 117018; D037342:Pertussis Toxin