Differential macrophage infiltration in early and advanced endometriosis and adjacent peritoneum.
OBJECTIVE
To investigate the distribution of macrophage (Mphi) infiltration in eutopic and ectopic endometrium throughout the menstrual cycle.


METHODS
Controlled clinical study using intact tissue.


METHODS
Nagasaki University School of Medicine, Nagasaki, Japan.


METHODS
Twenty infertile women with pelvic endometriosis and 20 women without endometriosis.


METHODS
Biopsy specimens from peritoneal lesions and corresponding eutopic endometrium were collected from women with or without endometriosis. Adjacent peritoneal biopsies were also obtained from a fraction of these women. The activated Mphi marker CD68, mitogenic marker hepatocyte growth factor (HGF), and endothelial cell surface marker von Willebrand factor were immunolocalized and quantitated by light microscopy and Q-H score.


METHODS
Tissue infiltration of Mphi in eutopic endometrium, ectopic endometrium, and adjacent peritoneum was examined, and its relationship with the immunoreaction of HGF and microvessel number was analyzed. The possible production of HGF by the isolated basal Mphi was also examined.


RESULTS
Tissue infiltration of Mphi in the eutopic and ectopic endometrium of women with stage I-II endometriosis was significantly higher than with stage III-IV endometriosis or in control women. Red peritoneal lesions and their adjacent peritoneum had the greatest Mphi concentration, compared with black or white lesions. These inflammatory cells showed a higher distribution in the secretory phase of the menstrual cycle. The Mphi density in the eutopic endometrium and corresponding red lesions showed a significant correlation with both Q-H score of HGF and microvessel density. A substantial amount of HGF was also produced by the isolated basal Mphi from women with endometriosis.


CONCLUSIONS
These results suggest that the peritoneal lesions of early and active endometriosis and their adjacent peritoneum harbor abundant Mphi that could be involved in the growth of endometriosis.
Khan
Khaleque Newaz
KN
Department of Obstetrics and Gynecology, Nagasaki University School of Medicine, Nagasaki, Japan. nemokhan@net.nagasaki-u.ac.jp
Masuzaki
Hideaki
H
Fujishita
Akira
A
Kitajima
Michio
M
Sekine
Ichiro
I
Ishimaru
Tadayuki
T
D000328:Adult; D001202:Ascitic Fluid / Q000737:chemistry / Q000473:pathology; D001808:Blood Vessels / Q000473:pathology; D018932:Chemokine CCL2 / Q000032:analysis; D018450:Disease Progression; D004715:Endometriosis / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D004717:Endometrium / Q000098:blood supply; D005260:Female; D017228:Hepatocyte Growth Factor / Q000096:biosynthesis / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000378:metabolism / Q000473:pathology*; D008597:Menstrual Cycle; D008833:Microcirculation; D009994:Osmolar Concentration; D010537:Peritoneum / Q000473:pathology*
D018932:Chemokine CCL2; D017228:Hepatocyte Growth Factor