Human Reproduction, Vol. 14, No. 12, 2944-2950,
December 1999
© 1999 European Society of Human Reproduction and Embryology
Endometrial ability to implant in ectopic sites can be prevented by interleukin-12 in a murine model of endometriosis
1 II Department of Obstetrics and Gynecology, University of Milano, 2 Department of Pathology, Istituti Clinici di Perfezionamento, 3 Roche Milano Ricerche and 4 Istituto Auxologico Italiano, Milano, Italy
Immune dysfunctions in endometriosis are widely documented but the effectiveness of immunotherapies for the management of the disease is still debated. Progress in this field has also been limited by the lack of an appropriate animal model of the disease. In this study, we created a model of endometriosis in immunocompetent mice to verify the ability of endometrium to implant in ectopic sites and to investigate the potential application of the cytokine interleukin (IL)-12 in preventing this ectopic implantation. Endometriotic lesions were induced in both C57BL/6 and BALB/c mice by inoculating syngenic endometrial fragments through a small laparotomic incision into the peritoneal space. All the animals challenged with syngenic endometrium showed evidence of peritoneal endometriosis at 3 weeks. Histologically, endometriotic lesions consisted of cystic endometrial glands surrounded by a stroma. Intraperitoneal injection of IL-12 was able to reduce total weight and total surface area of endometriotic lesions respectively of 77 and 61% in C57BL/6 and of 42 and 28% in BALB/c mice. These results demonstrate that IL-12 is able to induce a significant prevention of ectopic endometrial implantation in an in-vivo model of endometriosis. These findings support the possibility of using the immune system to generate novel therapies for the management of the disease.
Key words: ectopic implantation/endometriosis/interleukin-12/murine model
5 To whom correspondence should be addressed at: II Dept. Obstetrics and Gynecology, Via Commenda 12, 20122 Milan, Italy
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