Journal
REPRODUCTIVE SCIENCES
Volume 24, Issue 8, Pages 1121-1128Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/1933719117698584
Keywords
adhesions; inflammasome; interleukin 1; endometriosis; endometrium
Categories
Funding
- NIEHS [ES014942]
- Vanderbilt Medical Scholars Program
- NIH CTSA [UL1 RR 024975]
- [VA101 BX002583]
Ask authors/readers for more resources
Development of adhesions commonly occurs in association with surgery for endometriosis. Even in the absence of surgery, women with endometriosis appear to be at an enhanced risk of developing adhesions. In the current study, we utilized a chimeric mouse model of experimental endometriosis in order to examine the role of inflammasome activation in the development of postsurgical adhesions. Mice were randomized to receive peritoneal injections of human endometrial tissue fragments or endometrial tissue conditioned media (CM) from women with or without endometriosis 16 hours after ovariectomy and placement of an estradiol-releasing silastic capsule. A subset of mice receiving CM was also treated with interleukin (IL) 1 receptor antagonist (IL-1ra). Our studies demonstrate that peritoneal injection of endometrial tissue fragments near the time of surgery resulted in extensive adhesive disease regardless of tissue origin. However, adhesion scores were significantly higher in mice receiving CM from tissues acquired from patients with endometriosis compared to control tissue CM (P = .0001). Cytokine bead array analysis of endometrial CM revealed enhanced expression of IL-1 from patients with endometriosis compared to controls (P < .01). Finally, the ability of human tissue CM to promote adhesive disease was dramatically reduced in mice cotreated with IL-1ra (P < .0001). Our data implicate enhanced expression of IL-1 in women with endometriosis as a potential causal factor in their increased susceptibility of developing postsurgical adhesions. Thus, targeting inflammasome activation may be an effective strategy for the prevention of surgical adhesions in patients with endometriosis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available