Role of interleukin-32 in the pathogenesis of endometriosis: in vitro, human and transgenic mouse data

Mi-Young Lee, Mi‐Young Lee, Sung Hoon Kim, Young Sang Oh, Seung-Ho Heo, Seung‐Ho Heo, Kang-Hyun Kim, Hee Dong Chae, Chung‐Hoon Kim, Chung-Hoon Kim, Byung Moon Kang
Human Reproduction · 2018 · vol. 33(5) , pp. 807–816 · doi:10.1093/humrep/dey055 · PMID:29562285 · W2793277426
article OA: bronze CC0 ⤵ 28 in-corpus citations
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Interleukin-32 is elevated in endometriosis and promotes endometrial cell viability, proliferation, and invasion in vitro and in transgenic mouse models.

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Abstract

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.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Ascitic Fluid Endometriosis Endometrium Interleukins Adult Animals Ascitic Fluid Cell Line, Tumor Cell Proliferation Cell Proliferation Cell Survival Cell Survival Endometriosis Endometrium Female Humans Inflammation Inflammation Interleukins Interleukins

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