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The paper investigates whether Fusobacterium infection contributes to the development of endometriosis and examines how it affects endometrial fibroblasts, focusing on phenotypic transition driven by activated transforming growth factor–β (TGF-β) signaling. In a women’s cohort, Fusobacterium infiltration in the endometrium was reported in 64% of endometriosis patients versus <10% of controls, and experiments showed that Fusobacterium infection induced quiescent fibroblasts to transition to TAGLN-positive myofibroblasts with increased proliferative, adhesive, and migratory capacity in vitro. In a syngeneic mouse model, Fusobacterium inoculation increased TAGLN-positive myofibroblasts and led to more and heavier endometriotic lesions, while antibiotic treatment largely prevented establishment and reduced lesion burden; the caveat is that these findings are based on their cohort and animal/in vitro models rather than proving causality in all humans. This paper is centrally about endometriosis — specifically, it proposes a Fusobacterium-driven mechanism via TGF-β–mediated transition of endometrial fibroblasts to myofibroblasts that promotes ovarian endometriosis.
Abstract
Retrograde menstruation is a widely accepted cause of endometriosis. However, not all women who experience retrograde menstruation develop endometriosis, and the mechanisms underlying these observations are not yet understood. Here, we demonstrated a pathogenic role of Fusobacterium in the formation of ovarian endometriosis. In a cohort of women, 64% of patients with endometriosis but <10% of controls were found to have Fusobacterium infiltration in the endometrium. Immunohistochemical and biochemical analyses revealed that activated transforming growth factor–β (TGF-β) signaling resulting from Fusobacterium infection of endometrial cells led to the transition from quiescent fibroblasts to transgelin (TAGLN)–positive myofibroblasts, which gained the ability to proliferate, adhere, and migrate in vitro. Fusobacterium inoculation in a syngeneic mouse model of endometriosis resulted in a marked increase in TAGLN-positive myofibroblasts and increased number and weight of endometriotic lesions. Furthermore, antibiotic treatment largely prevented establishment of endometriosis and reduced the number and weight of established endometriotic lesions in the mouse model. Our data support a mechanism for the pathogenesis of endometriosis via Fusobacterium infection and suggest that eradication of this bacterium could be an approach to treat endometriosis.
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Fusobacterium infection facilitates the development of endometriosis through the phenotypic transition of endometrial fibroblasts
http://hdl.handle.net/2237/0002008401
http://hdl.handle.net/2237/000200840170b59901-6164-4d03-bf5a-25272b1b9f58
| 名前 / ファイル | ライセンス | アクション |
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combined.pdf (15.8 MB)
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| アイテムタイプ | itemtype_ver1(1) | |||||||||||||||||||||||||||||||||||||||
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| 公開日 | 2023-11-30 | |||||||||||||||||||||||||||||||||||||||
| タイトル | ||||||||||||||||||||||||||||||||||||||||
| タイトル | Fusobacterium infection facilitates the development of endometriosis through the phenotypic transition of endometrial fibroblasts | |||||||||||||||||||||||||||||||||||||||
| 言語 | en | |||||||||||||||||||||||||||||||||||||||
| 著者 |
Muraoka, Ayako
× Muraoka, Ayako
× Suzuki, Miho
× Hamaguchi, Tomonari
× Watanabe, Shinya
× Iijima, Kenta
× Murofushi, Yoshiteru
× Shinjo, Keiko
× Osuka, Satoko
× Hariyama, Yumi
× Ito, Mikako
× Ohno, Kinji
× Kiyono, Tohru
× Kyo, Satoru
× Iwase, Akira
× Kikkawa, Fumitaka
× Kajiyama, Hiroaki
× Kondo, Yutaka
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| アクセス権 | open access | |||||||||||||||||||||||||||||||||||||||
| アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||||||||||||||||||||||||||||||||||||
| 権利 | ||||||||||||||||||||||||||||||||||||||||
| 権利情報 | “This is the author’s version of the work. It is posted here by permission of the AAAS for personal use, not for redistribution. The definitive version was published in [Science Translational Medicine] on [v.15, n.700, 14 Jun 2023], DOI: [10.1126/scitranslmed.add1531].” | |||||||||||||||||||||||||||||||||||||||
| 言語 | en | |||||||||||||||||||||||||||||||||||||||
| 内容記述 | ||||||||||||||||||||||||||||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||||||||||||||||||||||||||||
| 内容記述 | Retrograde menstruation is a widely accepted cause of endometriosis. However, not all women who experience retrograde menstruation develop endometriosis, and the mechanisms underlying these observations are not yet understood. Here, we demonstrated a pathogenic role of Fusobacterium in the formation of ovarian endometriosis. In a cohort of women, 64% of patients with endometriosis but <10% of controls were found to have Fusobacterium infiltration in the endometrium. Immunohistochemical and biochemical analyses revealed that activated transforming growth factor–β (TGF-β) signaling resulting from Fusobacterium infection of endometrial cells led to the transition from quiescent fibroblasts to transgelin (TAGLN)–positive myofibroblasts, which gained the ability to proliferate, adhere, and migrate in vitro. Fusobacterium inoculation in a syngeneic mouse model of endometriosis resulted in a marked increase in TAGLN-positive myofibroblasts and increased number and weight of endometriotic lesions. Furthermore, antibiotic treatment largely prevented establishment of endometriosis and reduced the number and weight of established endometriotic lesions in the mouse model. Our data support a mechanism for the pathogenesis of endometriosis via Fusobacterium infection and suggest that eradication of this bacterium could be an approach to treat endometriosis. | |||||||||||||||||||||||||||||||||||||||
| 言語 | en | |||||||||||||||||||||||||||||||||||||||
| 出版者 | ||||||||||||||||||||||||||||||||||||||||
| 出版者 | American Association for the Advancement of Science | |||||||||||||||||||||||||||||||||||||||
| 言語 | en | |||||||||||||||||||||||||||||||||||||||
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| 言語 | eng | |||||||||||||||||||||||||||||||||||||||
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| 資源タイプresource | http://purl.org/coar/resource_type/c_6501 | |||||||||||||||||||||||||||||||||||||||
| タイプ | journal article | |||||||||||||||||||||||||||||||||||||||
| 出版タイプ | ||||||||||||||||||||||||||||||||||||||||
| 出版タイプ | AM | |||||||||||||||||||||||||||||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||||||||||||||||||||||||||||||||
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| 関連タイプ | isVersionOf | |||||||||||||||||||||||||||||||||||||||
| 識別子タイプ | DOI | |||||||||||||||||||||||||||||||||||||||
| 関連識別子 | https://doi.org/10.1126/scitranslmed.add1531 | |||||||||||||||||||||||||||||||||||||||
| 収録物識別子 | ||||||||||||||||||||||||||||||||||||||||
| 収録物識別子タイプ | PISSN | |||||||||||||||||||||||||||||||||||||||
| 収録物識別子 | 1946-6234 | |||||||||||||||||||||||||||||||||||||||
| 書誌情報 |
en : Science Translational Medicine 巻 15, 号 700, p. eadd1531, 発行日 2023-06-14 |
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