Impact of stress on mast cell and vitamin D receptor expression in an animal model of endometriosis (703.4)

Endometriosis is characterized by peritoneal inflammation, infertility and chronic pelvic pain that substantially affect quality of life. Since stress can affect the immune system and recruitment of inflammatory cells it may contribute to this condition. Vitamin D receptor (VDR) is associated with anti‐proliferative and anti‐inflammatory properties and is expressed in the cycling endometrium. AIM: Investigate the impact of stress on mast cells and VDR in an animal model of endometriosis. METHODS: Endometriosis was induced in female Sprague‐Dawley rats by suturing uterine horn tissue next to the intestinal mesentery. Sham rats had sutures only. Rats were exposed to either an uncontrollable or controllable stress protocol for 10 days (endo‐stress) or no stress (endo‐no stress). At sacrifice (day 60) all rats were examined for cysts. Colon and uterine tissue were analyzed for damage and myeloperoxidase (MPO) levels. Mast cell infiltration was measured by staining with toluidine blue or immunofluorescence, and VDR expression by immunohistochemistry. RESULTS: Endo‐stress rats developed more and bigger cysts than endo‐no stress rats. Uncontrollable stress resulted in higher colonic damage (p<0.05) and uterine MPO compared to no stress, while controllable stress showed no difference. Uncontrollable stress increased mast cell infiltration in colonic tissue compared to controllable stress (p<0.05), endo‐no stress (p<0.05) and sham‐no stress (p<0.01). There was increased mast cell infiltration in cysts. Endo‐no stress group had higher expression of VDR in uterus stroma nuclei and glands (p<0.05 vs controllable stress; p<0.05 vs sham, in glands only). CONCLUSION: Stress exacerbates development of cysts in an animal model of endometriosis through mechanisms involving mast cell recruitment, release of cell mediators and VDR down‐regulation. Grant Funding Source : Supported by R15AT006373 & R25GM082406