Effect of uncontrollable stress on the development of endometriosis and expression of S‐100 and COX‐2 in an animal model of endometriosis

The contribution of stress to the symptoms and progression of endometriosis, a chronic disease characterized by pain, peritoneal inflammation, adhesions and cysts, is unclear. AIM Examine the effect of stress on the expression of S‐100 (a marker for myelinated nerves) and COX‐2 (an enzyme catalyzing prostaglandin biosynthesis) in an animal model of endometriosis. METHODS Endometriosis was induced in female Sprague‐Dawley rats by suturing uterine horn implants next to the intestinal mesentery. Two weeks later one group (endo‐stress) was subjected to uncontrollable swim stress for 10 consecutive days. Endo‐control received no stress. Sham‐stress had sutures only then stress. Fecal pellets were counted during stress as a measure of anxiety. On day 60 all rats were examined for the presence of endometriotic vesicles, and the colons assessed for damage. Immunohistochemical analysis for S‐100 and COX‐2 expression was performed. RESULTS Exposure to stress increased the average vesicle length and their severity. No vesicles were found in sham‐stress. Stress increased colonic damage, motility, and numbers of mast cells (p<0.05). Increased positive staining for S‐100 and COX‐2 was found in colon and uterus in endo‐stress compared to endo‐control or sham‐stress. CONCLUSIONS Stress may exacerbate the development of vesicles in an animal model of endometriosis through mechanisms involving cell recruitment (eg. mast cells), and release of mediators such as prostaglandins.