Stress Exacerbates Endometriosis Manifestations and Inflammatory Parameters in an Animal Model

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Stress prior to endometriosis induction in rats increased vesicle severity, colonic inflammation, motility, and mast cell numbers, indicating stress exacerbates disease manifestations.

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This study used female Sprague-Dawley rats to test whether prior swim stress for 10 days alters the development and inflammatory profile of surgically induced endometriosis, comparing endo-stress rats to sham-stress (sutures only) and endo-no stress groups. On day 60, researchers quantified endometriotic vesicles and assessed colonic macroscopic and microscopic damage, while analyzing inflammatory cells in colonic tissue and peritoneal fluid. Stress exposure increased both the number and severity of endometriotic vesicles and was associated with greater colonic inflammation, motility, myeloperoxidase levels, and mast cell numbers, whereas endometriosis (regardless of stress) decreased central corticotropin-releasing factor immunoreactivity in the CA3 hippocampal subregion; the paper’s caveat is its reliance on an animal model and specified behavioral stress paradigm. This paper is centrally about endometriosis — it demonstrates that prior stress exacerbates endometriosis manifestations and associated inflammatory parameters in rats.

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Abstract

Women with endometriosis have significant emotional distress; however, the contribution of stress to the pathophysiology of this disease is unclear. We used a rat model of endometriosis to examine the effects of stress on the development of this condition and its influence on inflammatory parameters. Female Sprague-Dawley rats were subjected to swim stress for 10 consecutive days prior to the surgical induction of endometriosis by suturing uterine horn implants next to the intestinal mesentery (endo-stress). Sham-stress animals had sutures only, and an endo-no stress group was not subjected to the stress protocol. At the time of sacrifice on day 60, endometriotic vesicles were measured and colons assessed for macroscopic and microscopic damage. Colonic tissue and peritoneal fluid were collected for inflammatory cell analysis. Endometriosis, regardless of stress, produced a decrease in central corticotropin-releasing factor immunoreactivity, specifically in the CA3 subregion of the hippocampus. Prior exposure to stress increased both the number and severity of vesicles found in animals with endometriosis. Stress also increased colonic inflammation, motility, myeloperoxidase levels, and numbers of mast cells. In summary, prior stress may contribute to the development and severity of endometriosis in this animal model through mechanisms involving cell recruitment (eg, mast cells), release of inflammatory mediators, and deregulation of hypothalamic–pituitary axis responses in the hippocampus. Similar content being viewed by others

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Sci. 19, 851–862 (2012). https://doi.org/10.1177/1933719112438443 Published: Issue date: DOI: https://doi.org/10.1177/1933719112438443

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endometriosis

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Endometriosis Inflammation Stress, Psychological Animals Ascitic Fluid Ascitic Fluid Colon Colon Corticotropin-Releasing Hormone Corticotropin-Releasing Hormone Disease Models, Animal Endometriosis Endometriosis Endometriosis Female Hippocampus Hippocampus Inflammation Inflammation Mediators Inflammation Mediators

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