Oxytocin both increases proliferative response of peripheral blood lymphomonocytes to phytohemagglutinin and reverses immunosuppressive estrogen activity.
BACKGROUND
It has been shown that the neurohypophyseal peptide oxytocin is present in the human thymus and in vitro it can mimic interleukin (IL)-2 action in the induction of interferon-gamma production. In the present study, we tested the capacity of oxytocin to modulate the response of peripheral blood mononuclear cells (PBMCs) to phytohemagglutinin (PHA) and its ability to change the membrane expression of IL-2 receptor CD25 and the CD95 activation marker. Furthermore, whether oxytocin was able to reverse the inhibition of PBMC blastic response and CD25 expression induced by estradiol benzoate (E(2)B) was studied.


METHODS
Fifteen healthy women were studied with a mean age of 33.8 years, no previous pregnancies, all in the early follicular phase of the cycle with normal values of circulating estrogens.


RESULTS
The addition of oxytocin (1x10(-10) M, 1x10(-11) M, 1x10(-12) M) significantly increased the PBMC blastic response to PHA as well as the expression of both CD25 and CD95. These results were due to interaction of oxytocin with its specific receptor since the addition of an oxytocin antagonist completely reversed the oxytocin activity. In contrast, E(2)B induced a marked decrease of PHA-stimulated PBMC cell cycle progression and CD25 expression: the inhibitory effect of E(2)B was significantly counteracted by low concentrations of oxytocin.


CONCLUSIONS
The present results support the hypothesis that neuropeptides may act as a link in the network between the immune and the neuroendocrine systems.
Macciò
Antonio
A
Department of Obstetrics and Gynaecology, Sirai Hospital, 09013 Carbonia, Italy. a.maccio@tin.it
Madeddu
Clelia
C
Chessa
Paola
P
Panzone
Filomena
F
Lissoni
Paolo
P
Mantovani
Giovanni
G
D000328:Adult; D002455:Cell Division / Q000187:drug effects; D003270:Contraceptive Agents / Q000494:pharmacology; D004347:Drug Interactions; D004958:Estradiol / Q000031:analogs & derivatives* / Q000494:pharmacology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007376:Interleukin-2 / Q000494:pharmacology; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D008934:Mitogens / Q000494:pharmacology; D015213:Neuroimmunomodulation / Q000187:drug effects*; D010120:Oxytocics / Q000037:antagonists & inhibitors / Q000494:pharmacology; D010121:Oxytocin / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D010835:Phytohemagglutinins / Q000494:pharmacology*; D015375:Receptors, Interleukin-2 / Q000378:metabolism; D019014:fas Receptor / Q000378:metabolism
D003270:Contraceptive Agents; C508017:IL2RA protein, human; D007376:Interleukin-2; D053645:Interleukin-2 Receptor alpha Subunit; D008934:Mitogens; D010120:Oxytocics; D010835:Phytohemagglutinins; D015375:Receptors, Interleukin-2; D019014:fas Receptor; C074283:estradiol 3-benzoate; D004958:Estradiol; D010121:Oxytocin