title: Intraperitoneal inflammation decreases endometriosis in a mouse model.
abstract: BACKGROUND
  The role of the immune system in the pathogenesis of endometriosis remains elusive. It has been shown that patients have an altered peritoneal environment with increased levels of inflammatory cytokines, activated macrophages and reduced clearance of retrogradely transported endometrial fragments. However, it is not known if this unique inflammatory situation is cause or consequence of endometriosis. This study investigates the impact of a pre-existing peritoneal inflammation on endometriosis establishment in a mouse model.
  
  
  METHODS
  Endometriosis was induced by intraperitoneal injection of enhanced green fluorescent protein (EGFP)-expressing endometrium in mice. In parallel, a peritonitis model was established via intraperitoneal injection of thioglycolate medium (TM). Finally, endometriosis was induced in the inflamed peritoneal cavity and lesion establishment as well as morphological and histological characteristics were analysed.
  
  
  RESULTS
  Induction of endometriosis in an inflamed peritoneal cavity resulted in fewer lesions and significantly lower sum of lesion surface area per mouse in the TM-treated group. Additionally, a higher amount of non-attached debris could be detected in the peritoneal cavity of TM-treated mice.
  
  
  CONCLUSIONS
  An intraperitoneal inflammation decreases endometriosis establishment in this mouse model. Thus, a pre-existing peritoneal inflammation might not be a factor favouring the development of endometriosis.
authors.affiliation: GDD-TRG Women's Healthcare, Bayer Schering Pharma AG, Berlin, Germany.
authors.forename: N M
authors.initials: NM
authors.lastname: Nowak
authors.forename: O M
authors.initials: OM
authors.lastname: Fischer
authors.forename: T C
authors.initials: TC
authors.lastname: Gust
authors.forename: U
authors.initials: U
authors.lastname: Fuhrmann
authors.forename: U-F
authors.initials: UF
authors.lastname: Habenicht
authors.forename: A
authors.initials: A
authors.lastname: Schmidt
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004715:Endometriosis / Q000175:diagnosis* / Q000628:therapy*; D004717:Endometrium / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D049452:Green Fluorescent Proteins / Q000378:metabolism; D007107:Immune System; D007249:Inflammation / Q000175:diagnosis*; D008264:Macrophages / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010538:Peritonitis / Q000175:diagnosis; D013864:Thioglycolates / Q000378:metabolism
chemical_list: D016207:Cytokines; D013864:Thioglycolates; D049452:Green Fluorescent Proteins