Grant: Master's Award: Canada Graduate Scholarships

Endometriosis is a common gynaecological disease affecting between 6-10% of women. Due to stigma and misdiagnosis, patients wait on average 10.4 years before a diagnosis is achieved. There are currently no curative treatments for the disease. Symptoms include chronic pelvic pain, painful menstruation, and markedly decreased fertility. The disease is managed primarily through the use of hormonal contraceptives to reduce estrogen levels, a poor therapeutic option for patients wishing to pursue pregnancy. The primary cause of the disease is believed to be due to a process known as retrograde menstruation, whereby menstrual effluents travel backwards through the Fallopian tubes and implant in the pelvic cavity and develop a blood supply. It is likely that endometriosis is promoted by a dysfunctional immune system in which innate immune cells, such as macrophage, cannot mount the proper response to clear the refluxed menstrual debris. Elevated levels of several immune modulating signals have been identified in patients with endometriosis. It is therefore hypothesized that these signals alter that activation status of the macrophage. Macrophage are classically identified by there ability to promote inflammation and clear damaged cells by phagocytosis. However, in endometriosis, it is believed that the alternative activation of the macrophage reduce their ability to clear refluxed endometrial debris, and are the functional cells responsible for promoting the blood supply to the lesions through a wound repairing mechanism. Studying the molecular mechanisms responsible for alternative macrophage activation will yield an understanding of the environment conducive to endometriosis and generate targeted future immunotherapies.