title: Neutrophil depletion reduces endometriotic lesion formation in mice.
abstract: Neutrophils are known to be accumulated in endometriosis; however, direct evidence of the impact of neutrophils in the development of endometriosis was lacking. To clarify the importance of neutrophils, we examined the effect of neutrophil depletion on the development of endometriosis.
  
  
  
  Ovariectomized, estradiol-replaced, 8-week-old, female BALB/c mice were injected with endometrial fragments (Day 0). Neutrophils were depleted by anti-Gr-1 antibody, either in the early stage (from Day 1 to Day 3, group E) or late stage (from Day 8 to Day 12, group L). Control mice (group C) did not receive antibodies. On Day 14, mice were killed and the number and weight of endometriotic lesions were counted and weighed.
  
  
  
  The number of endometriotic lesions was significantly less in group E in comparison with Group C and Group L. Weight per lesion did not differ between groups.
  
  
  
  Neutrophils are essential for the initial formation of endometriosis.
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Masashi
authors.initials: M
authors.lastname: Takamura
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Kaori
authors.initials: K
authors.lastname: Koga
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Gentaro
authors.initials: G
authors.lastname: Izumi
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Yoko
authors.initials: Y
authors.lastname: Urata
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Miwako
authors.initials: M
authors.lastname: Nagai
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Akiko
authors.initials: A
authors.lastname: Hasegawa
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Miyuki
authors.initials: M
authors.lastname: Harada
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Hirata
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Hirota
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Osamu
authors.initials: O
authors.lastname: Wada-Hiraike
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Fujii
authors.affiliation: Obstetrics and Gynecology, the University of Tokyo, Tokyo, Japan.
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Osuga
mesh_terms: D000818:Animals; D000906:Antibodies / Q000633:toxicity; D004715:Endometriosis / Q000276:immunology* / Q000473:pathology; D005260:Female; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000276:immunology* / Q000473:pathology
chemical_list: D000906:Antibodies
keywords: Gr-1; endometriosis; mouse model