Interleukin-17A is present in neutrophils in endometrioma and stimulates the secretion of growth-regulated oncogene-α (Gro-α) from endometrioma stromal cells.
OBJECTIVE
To investigate a new role of interleukin (IL)-17A in endometriosis.


METHODS
Laboratory study.


METHODS
University hospital.


METHODS
Patients with ovarian endometrioma undergoing laparoscopy or laparotomy.


METHODS
Primary culture of endometrioma stromal cells (EoSCs) was stimulated with IL-17A. Sections of endometrioma tissue were immunostained with antibodies for IL-17A, growth-regulated oncogene-α (Gro-α), and elastase, a marker of neutrophils. They were also examined with immunofluorescent double staining for IL-17A and myeloperoxidase, another marker of neutrophils.


METHODS
Concentration of Gro-α was measured using a specific ELISA. Neutrophil chemotaxis was measured with Boyden chamber method. Immunostained sections were examined under microscope.


RESULTS
Interleukin-17A increased the secretion of Gro-α from EoSCs dose-dependently. The conditioned medium of EoSCs stimulated with IL-17A attracted more neutrophils than that of EoSCs stimulated with vehicle, and the increase was inhibited by the addition of Gro-α-neutralizing antibody. On immunostaining, IL-17A and Gro-α were detected in similar areas of the stroma beneath the epithelium, where Gro-α was detected in cells with a stromal cell appearance whereas IL-17A was detected in neutrophils as determined by detection of elastase. Fluorescent immunostaining corroborated that myeloperoxidase-positive neutrophils were also positive for IL-17A.


CONCLUSIONS
It is suggested that IL-17A produced by neutrophils stimulates Gro-α secretion from EoSCs, thereby recruiting more neutrophils and inducing perpetuating inflammation in endometriosis.
Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Masashi
M
Takamura
Yutaka
Y
Osuga
Gentaro
G
Izumi
Osamu
O
Yoshino
Kaori
K
Koga
Ako
A
Saito
Tetsuya
T
Hirata
Yasushi
Y
Hirota
Miyuki
M
Harada
Akiko
A
Hasegawa
Yuji
Y
Taketani
D002478:Cells, Cultured; D054360:Chemokine CXCL1 / Q000378:metabolism*; D002634:Chemotaxis, Leukocyte; D017077:Culture Media, Conditioned / Q000378:metabolism; D004715:Endometriosis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D004717:Endometrium / Q000276:immunology / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005455:Fluorescent Antibody Technique; D006785:Hospitals, University; D006801:Humans; D007150:Immunohistochemistry; D020381:Interleukin-17 / Q000378:metabolism*; D007564:Japan; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D019899:Paracrine Communication; D017154:Stromal Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
C475829:CXCL1 protein, human; D054360:Chemokine CXCL1; D017077:Culture Media, Conditioned; C508717:IL17A protein, human; D020381:Interleukin-17