Literature DB >> 3260616

Immunohistochemical characterization of the estrogen-stimulated leukocyte influx in the immature rat uterus.

Y Zheng1, Z Z Zhou, C R Lyttle, C Teuscher.   

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.

Entities:  

Mesh:

Substances:

Year:  1988        PMID: 3260616     DOI: 10.1002/jlb.44.1.27

Source DB:  PubMed          Journal:  J Leukoc Biol        ISSN: 0741-5400            Impact factor:   4.962


  4 in total

1.  Evidence for the genetic control of estradiol-regulated responses. Implications for variation in normal and pathological hormone-dependent phenotypes.

Authors:  J S Griffith; S M Jensen; J K Lunceford; M W Kahn; Y Zheng; E A Falase; C R Lyttle; C Teuscher
Journal:  Am J Pathol       Date:  1997-06       Impact factor: 4.307

2.  Regulated expression of matrix metalloproteinases, inflammatory mediators, and endometrial matrix remodeling by 17beta-estradiol in the immature rat uterus.

Authors:  Louise A Russo; Bryan J Peano; Shreya P Trivedi; Todd D Cavalcanto; Benjamin A Olenchock; Joseph A Caruso; Amanda R Smolock; Oleg Vishnevsky; Russell M Gardner
Journal:  Reprod Biol Endocrinol       Date:  2009-11-04       Impact factor: 5.211

3.  Immunohistochemical localization of the eosinophil major basic protein in the uterus horn and cervix of the rat at term and after parturition.

Authors:  M J Duchesne; E Badia
Journal:  Cell Tissue Res       Date:  1992-10       Impact factor: 5.249

4.  Recombineering-based dissection of flanking and paralogous Hox gene functions in mouse reproductive tracts.

Authors:  Anna M Raines; Mike Adam; Bliss Magella; Sara E Meyer; H Leighton Grimes; Sudhansu K Dey; S Steven Potter
Journal:  Development       Date:  2013-06-12       Impact factor: 6.868

  4 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.