Induction of endometriosis in the mouse inhibits spleen leukocyte function

Background. It is still unclear whether the immunologic perturbation observ ed in women with endometriosis represents an intrinsic defect of the immune system or it is consequent to the presence of endometrium in ectopic sites . The present study was aimed to evaluate the immunoregulatory properties o f ectopic endometrial implants in a model of experimental endometriosis in mice. Methods. Endometriosis was induced in n=10 mice by inoculating endometrial fragments obtained from syngenic donor mice into the peritoneal space. Twel ve mice were similarly treated but were not inoculated with endometrium and were used as control mice. At an explorative laparotomy performed in all t he animals after three weeks, the extent of peritoneal lesions, when presen t, was evaluated by weight assessment and surface area measurement. In both mice that were inoculated with endometrium and control animals, spleens we re removed. The effect of endometriosis induction on concanavalin A-induced spleenocyte proliferation was investigated. Results. A significant inhibition of spleenocyte growth was demonstrated in mice in which endometriosis was induced (36156+/-3061 cpm) compared to con trol animals (47172+/-3210 cpm: p<0.05). Moreover. a significant inverse co rrelation was found between spleenocyte proliferation and weight and surfac e area of the peritoneal endometriotic lesions (r=0.76; p<0.02 and r=0.75: p<0.02, respectively). Conclusion. These findings suggest that the presence of ectopic endometrial implants within the peritoneal cavity leads to substantial changes of the immune response in vivo. These changes may have significant implications fo r the understanding of the etiopathogenesis of endometriosis.