No abstract

Intraperitoneal injection of endometrial tissues into inbred mice such as C57BL/6J is widely used as a model to study endometriosis, a disease characterized by the abnormal proliferation of endometrial cells which invade various tissues within the peritoneal cavity. However, most of these inbred mouse strains have a weak immune system and are often ovariectomized, which is not reflective of the human population in general. Hence, this study used the ovary intact ICR mouse strain as a model to study the immune response during endometriosis development using a non-surgical syngeneic model with no estrogen supplementation. We showed that ICR mice developed ectopic endometrial tissues after 8 wk, but these were mostly necrotic. Reducing the induction period to 4 wk increased the number of ectopic tissues, and endometriotic lesions were also formed in 30% of the induced recipient mice, albeit with a relatively low incidence rate. Endometriotic lesions in ICR mice were also associated with fewer lesion-resident macrophages and lesser vascularization than in C57BL/6J mice. This is further supported by a significantly downregulated expression of genes involved in angiogenesis and M2 macrophage activity in ICR versus C57BL/6J donor endometrium. Conversely, inflammatory response genes were significantly upregulated in the endometrium of ICR versus C57BL/6J mice. Overall, these data implicate the role of inflammation in inhibiting the establishment of endometrial lesions in ICR mice and the involvement of macrophage in promoting endometriosis in C57BL/6J mice. The present work reports the establishment of endometriotic lesions in outbred ICR mice by a less invasive syngeneic intraperitoneal injection procedure.

No abstract

No abstract