The pathophysiology of intestinal endometriosis is exacerbated by uncontrollable stress

It is not known whether stress affects the severity of endometriosis in women. Aim: Assess the effects of chronic stress in an established animal model of intestinal endometriosis. Methods: Endometriosis was surgically induced in female rats. One group of rats (endo‐stress) was subjected to uncontrollable swim stress for 10 consecutive days. Endo‐controls had endometriosis with no stress. Sham‐stress had sutures only then swim stress. On day 60 all rats were sacrificed and examined for the presence of endometriotic vesicles. The colons were removed and assessed for macroscopic damage, myeloperoxidase (MPO) activity and histology. Results: None of the sham‐stress animals developed vesicles. The endo‐control rats developed vesicles with an average total vesicle length of 6.57 ± 0.96mm per animal. This was increased to 11.26 ± 5.27mm in the endo‐stress group (n=3‐4 ± sem). The endo‐control rats had higher macroscopic and histological colonic damage scores than the sham‐stress animals, which was increased further by stress. The endo‐stress also had the shortest colon length, increased numbers of colonic mast cells, higher MPO levels, and an increase in peritoneal fluid cell infiltration. Conclusions: This study presents evidence for the first time of the negative consequences of stress in the progression of endometriosis, most likely through an effect on the immune system. 2G12RR03050, SO6GM00823 & R01HD050559