Functional and phenotypic alterations in peritoneal macrophages from patients with early and advanced endometriosis.
The aim of this study was to elucidate whether peritoneal macrophage (pMO) alterations are a generalized feature in all stages of endometriosis and the effect of hormonal treatment on this leukocyte population. For this purpose we quantified the number of pMO, the expression of HLA-DR antigen (pMO DR+), percentages of pMO that reduced nitro-blue tetrazolium (pMO NBT+), and interleukin-1 (IL-1) and prostaglandin E2 (PGE2) production by pMO from patients with early (stages I/II) and advanced (stages III/IV) endometriosis, we also analyzed some of these properties in pMO from patients which had been treated for 6 months with 800 mg/day of Danazol or gonadotropin releasing hormone agonist (GnRHa). We found that there were a significant increase of the pMO number in both types of patients, though the highest values were obtained in early endometriosis (p < 0.001). Percentages of pMO DR+ were decreased in all patients (p < 0.01) while percentages of pMO NBT+ were significantly increased. Production of IL-1 by early and advanced endometriosis pMO were considerably enhanced. PGE2 release was not altered in early endometriosis pMO but, in advanced endometriosis, pMO PGE2 levels were 100-fold higher than control values. In posttreatment patients, the number of pMO and percentage of pMO NBT+ were similar to early endometriosis patients, though the percentage of pMO DR+ was within the normal range. We conclude that the pMO population, as well as IL-1 and PGE2 production, were altered in all stages of endometriosis, and that these changes could be involved in the pathogenesis of endometriosis and associated infertility. Hormonal treatments do not reverse the pMO changes.
Raiter-Tenenbaum
A
A
Instituto de Biología y Medicina Experimental-CONICET, Buenos Aires, Argentina.
Barañao
R I
RI
Etchepareborda
J J
JJ
Meresman
G F
GF
Rumi
L S
LS
D000328:Adult; D003613:Danazol / Q000627:therapeutic use; D015232:Dinoprostone / Q000378:metabolism; D004715:Endometriosis / Q000188:drug therapy / Q000276:immunology*; D004965:Estrogen Antagonists / Q000627:therapeutic use; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists; D006684:HLA-DR Antigens / Q000145:classification; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism; D008262:Macrophage Activation / Q000187:drug effects / Q000276:immunology; D008264:Macrophages / Q000145:classification / Q000187:drug effects / Q000276:immunology*; D009580:Nitroblue Tetrazolium / Q000378:metabolism; D010587:Phagocytosis / Q000187:drug effects / Q000276:immunology; D010641:Phenotype
D004965:Estrogen Antagonists; D006684:HLA-DR Antigens; D007375:Interleukin-1; D009580:Nitroblue Tetrazolium; D007987:Gonadotropin-Releasing Hormone; D015232:Dinoprostone; D003613:Danazol