Sperm phagocytosis by human peritoneal macrophages: a possible cause of infertility in endometriosis.

Published

Journal Article

The mechanism of infertility in women with endometriosis is unknown, but it is independent of mechanical factors that affect fallopian tube function. Increased numbers of peritoneal macrophages are present in women with endometriosis and have access to the female reproductive tract via the oviducts. To determine whether peritoneal macrophages might phagocytize sperm and thereby contribute to infertility in women with endometriosis, we examined peritoneal macrophages from 32 fertile and infertile women; the infertile group was separated into those with and those without visible endometriosis. Peritoneal macrophages from infertile patients with endometriosis phagocytized more normal sperm in vitro (84% +/- 4%) than did those from fertile women (43% +/- 4%) or infertile women without endometriosis (46% +/- 8%) (p less than 0.002). The sperm phagocytosis occurred rapidly and reached a peak by approximately 6 hours. Incubation at 0 degrees C, lysing the macrophages by freezing and thawing, or fixing the macrophages with glutaraldehyde inhibited the sperm uptake by macrophages. The process occurred in cultures with or without serum, thereby indicating that the sperm phagocytosis was not dependent on sperm opsonization with a serum factor. Electron microscopy showed internalization of the spermatozoa into phagosomes with subsequent intravacuolar degradation. These data demonstrate that: (1) peritoneal macrophages phagocytize and degrade sperm in vitro and (2) peritoneal macrophages isolated from women with endometriosis exhibit greater phagocytosis in vitro than do macrophages from fertile women or infertile women without endometriosis. These results suggest that, if peritoneal macrophages from women with endometriosis enter the reproductive tract via the oviducts, they might adversely influence fertilization by phagocytizing sperm.

Full Text

Duke Authors

Cited Authors

  • Muscato, JJ; Haney, AF; Weinberg, JB

Published Date

  • November 1, 1982

Published In

Volume / Issue

  • 144 / 5

Start / End Page

  • 503 - 510

PubMed ID

  • 6753586

Pubmed Central ID

  • 6753586

Electronic International Standard Serial Number (EISSN)

  • 1097-6868

International Standard Serial Number (ISSN)

  • 0002-9378

Digital Object Identifier (DOI)

  • 10.1016/0002-9378(82)90217-4

Language

  • eng