Study Question: Does interleukin-32 (IL-32) play a role in the pathogenesis of endometriosis?
Summary Answer: IL-32 might be involved in the pathogenesis of endometriosis through increased viability, proliferation and invasion of endometrial cells.
What Is Known Already: Endometriosis is characterized as a chronic inflammatory disease and several proinflammatory cytokines are suggested to be involved in its pathogenesis and pathophysiology. IL-32, recognized as a new proinflammatory cytokine and a strong inducer of other proinflammatory cytokines, has been shown to serve as a key modulator in several chronic inflammatory diseases.
Study Design, Size, Duration: This study included comparison of IL-32 levels in the peritoneal fluids between women with and without endometriosis, in-vitro experiments using Ishikawa cells and endometrial stromal cells (ESCs), and experiments on IL-32 transgenic mice and wild-type mice with induced endometriosis.
Participants/materials, Setting, Methods: IL-32 levels in the peritoneal fluids were measured using enzyme-linked immunosorbent assays. Cell viability, expression of proliferating cell nuclear antigen (PCNA), and cellular invasiveness were analyzed following in-vitro treatment of Ishikawa cells and ESCs with recombinant IL-32 alpha (α) and gamma (γ). Ectopic endometriotic lesions were compared between IL-32 transgenic mice and wild-type mice after autologous endometrial transplantation with immunohistochemistry for Ki-67 antigen and PCNA.
Main Results And The Role Of Chance: The peritoneal fluid concentration of IL-32 was significantly higher in patients with advanced stage endometriosis compared with the controls. In-vitro treatment with IL-32 α and γ caused significant increases in cellular viability, PCNA expression, and invasiveness in Ishikawa cells and ESCs. The IL-32 transgenic mice had a significantly larger size of the ectopic endometrial lesions with higher expression of Ki-67 antigen and PCNA compared with wild-type mice.
Large Scale Data: N/A.
Limitations, Reasons For Caution: It is still unclear whether IL-32 is a main regulator, or one of several downstream proinflammatory cytokines, causing establishment and/or progression of endometriosis.
Wider Implications Of The Findings: Further investigation on IL-32 signaling pathways may contribute to development a more effective treatment of endometriosis.
Study Funding/competing Interest(s): This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant number: HI16C1682). None of the authors has anything to disclose.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1093/humrep/dey055 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!