Production of macrophage inflammatory protein-3alpha in human follicular fluid and cultured granulosa cells.
OBJECTIVE
To investigate the role of macrophage inflammatory protein (MIP)-3alpha in human ovulation.


METHODS
Study of the levels of MIP-3alpha in serum and follicular fluid. The effects of interleukin (IL)-1alpha, IL-1 receptor antagonist (RA), and tumor necrosis factor (TNF)-alpha on the secretion of MIP-3alpha by primary cultured granulosa-lutein cells and an immortalized granulosa cell line (GC1a) were investigated.


METHODS
Research laboratory at a university medical school.


METHODS
Forty-six patients with sterility undergoing in vitro fertilization and embryo transfer (i.v.f.-ET).


METHODS
Follicular fluid was obtained from study participants, and granulosa-lutein cells and GC1a were incubated with IL-1alpha, IL-1RA, or TNF-alpha for 4 to 32 hours.


METHODS
The concentration of MIP-3alpha in human follicular fluid was measured and correlated with oocyte maturation. We also cultured granulosa cells and examined the regulation of MIP-3alpha production. The concentrations of MIP-3alpha in the serum, follicular fluid, and culture medium were measured using enzyme-linked immunoabsorbent assay.


RESULTS
Concentrations of MIP-3alpha were significantly higher in the follicular fluid, but it was not detected in the serum. Concentrations of MIP-3alpha were statistically significantly higher in the follicular fluid containing mature oocytes than in follicular fluid containing immature oocytes. The production of MIP-3alpha was markedly increased over the basal level after treatment with IL-1alpha and TNF-alpha in a dose-dependent manner. The stimulatory effect of IL-1alpha was inhibited by IL-1RA.


CONCLUSIONS
Our data suggest that MIP-3alpha was present in follicular fluid and correlated with oocyte maturation, and was regulated by IL-1alpha and TNF-alpha. Thus, MIP-3alpha may play an important role in the human preovulatory process.
Kawano
Yasushi
Y
Department of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Oita, Japan. kawayas@med.oita-u.ac.jp
Fukuda
Junichiro
J
Nasu
Kaei
K
Nishida
Masakazu
M
Narahara
Hisashi
H
Miyakawa
Isao
I
D000328:Adult; D002461:Cell Line, Transformed; D002478:Cells, Cultured; D016922:Cellular Senescence; D054418:Chemokine CCL20; D019742:Chemokines, CC / Q000096:biosynthesis* / Q000097:blood; D003338:Corpus Luteum / Q000378:metabolism / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D005260:Female; D015571:Follicular Fluid / Q000378:metabolism*; D006107:Granulosa Cells / Q000378:metabolism*; D006801:Humans; D007247:Infertility, Female / Q000378:metabolism* / Q000473:pathology; D007375:Interleukin-1 / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000494:pharmacology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis* / Q000097:blood; D009865:Oocytes; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D014409:Tumor Necrosis Factor-alpha / Q000008:administration & dosage / Q000494:pharmacology
C108355:CCL20 protein, human; D054418:Chemokine CCL20; D019742:Chemokines, CC; D007375:Interleukin-1; D019402:Macrophage Inflammatory Proteins; D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha