Monocyte-mediated enhancement of endometrial cell proliferation in women with endometriosis.
OBJECTIVE
To investigate the capacity of monocytes from women with endometriosis to influence endometrial cell proliferation.


METHODS
Uterine endometrial cells were cultured in the presence and absence of autologous blood monocytes for 72 hours before assessment of endometrial cell proliferation by thymidine incorporation.


METHODS
Patients were tested at initial presentation for evaluation of infertility and/or endometriosis.


METHODS
Fertile controls, n = 17; infertile controls, n = 9; untreated endometriosis, n = 29.


METHODS
None.


RESULTS
Endometrial cell proliferation was enhanced significantly by blood monocytes in patients with endometriosis but was suppressed significantly by blood monocytes in fertile controls. Endometrial cell proliferation was not affected significantly by blood monocytes in infertile controls analyzed as a group, but a subset of infertile patients also showed enhancement of endometrial cell proliferation by blood monocytes.


CONCLUSIONS
Blood monocytes from patients with endometriosis and a subset of patients with unexplained infertility enhance autologous endometrial cell proliferation, whereas blood monocytes from fertile patients suppress endometrial cell proliferation. The capacity of monocytes to enhance endometrial cell proliferation appears to require both monocyte-derived factors that stimulate endometrial cell proliferation and endometrial cells capable of responding to those stimulatory factors. If either of these factors is absent, monocytes either suppress or have no effect on endometrial cell proliferation.
Braun
D P
DP
Department of Medicine, Rush Medical College, Chicago, Illinois 60612.
Muriana
A
A
Gebel
H
H
Rotman
C
C
Rana
N
N
Dmowski
W P
WP
D000328:Adult; D002455:Cell Division / Q000502:physiology; D004715:Endometriosis / Q000150:complications / Q000473:pathology*; D004717:Endometrium / Q000473:pathology*; D005260:Female; D006801:Humans; D007246:Infertility / Q000209:etiology; D009000:Monocytes / Q000502:physiology*; D014591:Uterine Diseases / Q000473:pathology*