[Changes in the systemic immunologic response in association with endometriosis using an animal model]

Ginecol Obstet Mex. 2002 Apr:70:171-81.
[Article in Spanish]

Abstract

Introduction: Endometriosis constitutes the growth of endometrial tissue in a place other than the uterine cavity. Its etiopathogenesis is unknown, although there is some evidence associating it with the decrease of cytotoxic activity in the immunological system.

Objective: Evaluating the relationship between the development of ectopic endometrial tissue and the immunological status, and enumerating lymphocyte subpopulations and cytokine synthesis in T lymphocytes, using a murine endometriosis model.

Methodology: Spleen lymphocytes isolated from two study groups of 10 female mice of the Balb/c strain that had been submitted to the surgical implantation of autologous endometrial tissue in the peritoneal cavity, and sacrificed after 5 (group I) and 8 (group II) weeks, were incubated--or not--with PMA/lonomicine. Lymphocyte T numbers and their cytokine production were determined by flow cytometry.

Results: A lower dispersion of the ectopic tissue growth value was observed in group II (24% vs. 42%). A smaller population of cytotoxic T lymphocytes and a greater IL-4 production in the stimulated cells of the study group (p < 0.05) were observed, as compared to the control group.

Conclusions: The presence of endometrial tissue in the uterine cavity decreases the amount of cytotoxic T lymphocytes and increases IL-4 production in total T lymphocytes, suggesting a modulation of the systemic immunological response to TH-2.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Endometriosis / immunology*
  • Female
  • Immunity, Cellular
  • Interferon-gamma / metabolism*
  • Interleukin-10 / metabolism
  • Interleukin-2 / metabolism
  • Interleukin-4 / metabolism
  • Interleukins / metabolism*
  • Mice
  • Mice, Inbred BALB C
  • Models, Animal
  • T-Lymphocyte Subsets*
  • T-Lymphocytes / immunology*

Substances

  • Interleukin-2
  • Interleukins
  • Interleukin-10
  • Interleukin-4
  • Interferon-gamma