title: Seminal plasma components stimulate interleukin-8 and interleukin-10 release.
abstract: Human seminal plasma has potent anti-inflammatory properties which are thought to confer a survival advantage to the spermatozoa within the hostile female genital tract. In contrast, a profound pro-inflammatory leukocytosis has been observed post-coitus in animals and humans. Whether components of seminal plasma are involved in initiating this leukocytic reaction is not known. This study investigated the effect of human seminal plasma, a seminal plasma fraction and its principal constituent prostaglandins, prostaglandin E2 (PGE2) and 19-hydroxy PGE, on the release of the pro-inflammatory neutrophil chemotactic factor interleukin-8 (IL-8) and the anti-inflammatory cytokines interleukin-10 (IL-10) and secretory leukocyte protease inhibitor (SLPI). The tissues studied were non-pregnant cervical explants, peripheral blood and the monocyte cell line U937. Seminal plasma fraction (SPF) significantly (P < 0.05) stimulated release of IL-8 and inhibited release of SLPI from non-pregnant cervical explants. SPF, PGE2 and 19-hydroxy PGE significantly (P< 0.005) stimulated IL-8 release from peripheral blood and U937 cells. 19-hydroxy PGE was significantly (P< 0.005) more effective than PGE2 in stimulating IL-8 release. Seminal plasma, SPF and PGE2 significantly (P < 0.05) stimulated IL-10 release from U937 cells. 19-hydroxy PGE stimulated IL-10 release from U937 cells but this failed to reach significance. Release of IL-10 by cervical explants and SLPI by peripheral blood and U937 cells were below the detection limit of the assays employed. We suggest that the anti- and pro-inflammatory immune responses which seminal plasma induces might act in combination initially to promote sperm survival and then to facilitate their removal from the female genital tract.
authors.affiliation: Department of Obstetrics and Gynaecology, University of Edinburgh, Centre for Reproductive Biology, UK.
authors.forename: F C
authors.initials: FC
authors.lastname: Denison
authors.forename: V E
authors.initials: VE
authors.lastname: Grant
authors.forename: A A
authors.initials: AA
authors.lastname: Calder
authors.forename: R W
authors.initials: RW
authors.lastname: Kelly
mesh_terms: D000328:Adult; D000527:Alprostadil / Q000031:analogs & derivatives / Q000378:metabolism; D001769:Blood / Q000187:drug effects / Q000378:metabolism; D002457:Cell Extracts / Q000494:pharmacology; D002460:Cell Line; D002584:Cervix Uteri / Q000187:drug effects / Q000378:metabolism*; D015232:Dinoprostone / Q000031:analogs & derivatives / Q000378:metabolism / Q000494:pharmacology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D016753:Interleukin-10 / Q000378:metabolism*; D016209:Interleukin-8 / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D053491:Proteinase Inhibitory Proteins, Secretory; D011506:Proteins / Q000378:metabolism; D053481:Secretory Leukocyte Peptidase Inhibitor; D012661:Semen / Q000502:physiology*
chemical_list: D002457:Cell Extracts; D016209:Interleukin-8; D053491:Proteinase Inhibitory Proteins, Secretory; D011506:Proteins; C506814:SLPI protein, human; D053481:Secretory Leukocyte Peptidase Inhibitor; D016753:Interleukin-10; C025128:19-hydroxyprostaglandin E1; C048823:19-hydroxyprostaglandin E2; D000527:Alprostadil; D015232:Dinoprostone