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Interleukin-33 modulates inflammation in endometriosis
Endometriosis is a debilitating condition that is categorized by the abnormal growth of endometrial tissue outside the uterus. Although the pathogenesis of this disease remains unknown, it is well established that endometriosis patients exhibit immune dysfunction. Interleukin (IL)-33 is a danger sig...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5738435/ https://www.ncbi.nlm.nih.gov/pubmed/29263351 http://dx.doi.org/10.1038/s41598-017-18224-x |
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author | Miller, Jessica E. Monsanto, Stephany P. Ahn, Soo Hyun Khalaj, Kasra Fazleabas, Asgerally T. Young, Steven L. Lessey, Bruce A. Koti, Madhuri Tayade, Chandrakant |
author_facet | Miller, Jessica E. Monsanto, Stephany P. Ahn, Soo Hyun Khalaj, Kasra Fazleabas, Asgerally T. Young, Steven L. Lessey, Bruce A. Koti, Madhuri Tayade, Chandrakant |
author_sort | Miller, Jessica E. |
collection | PubMed |
description | Endometriosis is a debilitating condition that is categorized by the abnormal growth of endometrial tissue outside the uterus. Although the pathogenesis of this disease remains unknown, it is well established that endometriosis patients exhibit immune dysfunction. Interleukin (IL)-33 is a danger signal that is a critical regulator of chronic inflammation. Although plasma and peritoneal fluid levels of IL-33 have been associated with deep infiltrating endometriosis, its contribution to the disease pathophysiology is unknown. We investigated the role of IL-33 in the pathology of endometriosis using patient samples, cell lines and a syngeneic mouse model. We found that endometriotic lesions produce significantly higher levels of IL-33 compared to the endometrium of healthy, fertile controls. In vitro stimulation of endometrial epithelial, endothelial and endometriotic epithelial cells with IL-33 led to the production of pro-inflammatory and angiogenic cytokines. In a syngeneic mouse model of endometriosis, IL-33 injections caused systemic inflammation, which manifested as an increase in plasma pro-inflammatory cytokines compared to control mice. Furthermore, endometriotic lesions from IL-33 treated mice were highly vascularized and exhibited increased proliferation. Collectively, we provide convincing evidence that IL-33 perpetuates inflammation, angiogenesis and lesion proliferation, which are critical events in the lesion survival and progression of endometriosis. |
format | Online Article Text |
id | pubmed-5738435 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57384352017-12-22 Interleukin-33 modulates inflammation in endometriosis Miller, Jessica E. Monsanto, Stephany P. Ahn, Soo Hyun Khalaj, Kasra Fazleabas, Asgerally T. Young, Steven L. Lessey, Bruce A. Koti, Madhuri Tayade, Chandrakant Sci Rep Article Endometriosis is a debilitating condition that is categorized by the abnormal growth of endometrial tissue outside the uterus. Although the pathogenesis of this disease remains unknown, it is well established that endometriosis patients exhibit immune dysfunction. Interleukin (IL)-33 is a danger signal that is a critical regulator of chronic inflammation. Although plasma and peritoneal fluid levels of IL-33 have been associated with deep infiltrating endometriosis, its contribution to the disease pathophysiology is unknown. We investigated the role of IL-33 in the pathology of endometriosis using patient samples, cell lines and a syngeneic mouse model. We found that endometriotic lesions produce significantly higher levels of IL-33 compared to the endometrium of healthy, fertile controls. In vitro stimulation of endometrial epithelial, endothelial and endometriotic epithelial cells with IL-33 led to the production of pro-inflammatory and angiogenic cytokines. In a syngeneic mouse model of endometriosis, IL-33 injections caused systemic inflammation, which manifested as an increase in plasma pro-inflammatory cytokines compared to control mice. Furthermore, endometriotic lesions from IL-33 treated mice were highly vascularized and exhibited increased proliferation. Collectively, we provide convincing evidence that IL-33 perpetuates inflammation, angiogenesis and lesion proliferation, which are critical events in the lesion survival and progression of endometriosis. Nature Publishing Group UK 2017-12-20 /pmc/articles/PMC5738435/ /pubmed/29263351 http://dx.doi.org/10.1038/s41598-017-18224-x Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Miller, Jessica E. Monsanto, Stephany P. Ahn, Soo Hyun Khalaj, Kasra Fazleabas, Asgerally T. Young, Steven L. Lessey, Bruce A. Koti, Madhuri Tayade, Chandrakant Interleukin-33 modulates inflammation in endometriosis |
title | Interleukin-33 modulates inflammation in endometriosis |
title_full | Interleukin-33 modulates inflammation in endometriosis |
title_fullStr | Interleukin-33 modulates inflammation in endometriosis |
title_full_unstemmed | Interleukin-33 modulates inflammation in endometriosis |
title_short | Interleukin-33 modulates inflammation in endometriosis |
title_sort | interleukin-33 modulates inflammation in endometriosis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5738435/ https://www.ncbi.nlm.nih.gov/pubmed/29263351 http://dx.doi.org/10.1038/s41598-017-18224-x |
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