RRC ID |
76704
|
著者 |
Muraoka A, Suzuki M, Hamaguchi T, Watanabe S, Iijima K, Murofushi Y, Shinjo K, Osuka S, Hariyama Y, Ito M, Ohno K, Kiyono T, Kyo S, Iwase A, Kikkawa F, Kajiyama H, Kondo Y.
|
タイトル |
Fusobacterium infection facilitates the development of endometriosis through the phenotypic transition of endometrial fibroblasts.
|
ジャーナル |
Sci Transl Med
|
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.
|
巻・号 |
15(700)
|
ページ |
eadd1531
|
公開日 |
2023-6-14
|
DOI |
10.1126/scitranslmed.add1531
|
PMID |
37315109
|
MeSH |
Animals
Disease Models, Animal
Endometriosis*
Endometrium
Female
Fibroblasts
Fusobacterium Infections*
Humans
Mice
Myofibroblasts
|
IF |
16.304
|
リソース情報 |
遺伝子材料 |
Genome Network Project Human cDNA clone IRAK141P09 (HGX056769) |