INVESTIGADORES
LAROCCA Luciana
congresos y reuniones científicas
Título:
Deficiencies in VIP levels during the feto-maternal dialogue conditioned the pregnancy outcome
Autor/es:
FRACCAROLI L; LAROCCA L; CALAFAT M; ROCA V; PEREZ LEIROS C; RAMHORST R
Lugar:
Orlando
Reunión:
Congreso; 29th Annual meeting of the American Society of Reproductive Immunology.; 2009
Resumen:
Successful embryo implantation occurs followed by a
local pro-inflammatory and Th1 response, subsequently
controlled by a Th2 response. VIP (vasoactive
intestinal peptide) favors tolerance to fetal
antigens displaying anti-inflammatory effects and
promoting tolerogenic/Th2 responses. Since a potential
exacerbated pro-inflammatory/Th1 response
could be implicated into immunological abortion
failures, we investigated whether VIP could control
the initial pro-inflammatory response in patients
with recurrent spontaneous abortions (RSA). We
tested VIP effects on maternal PBMCs (from RSA
and fertile women) after interaction with immortalized
trophoblast cells (Swan 71) as representative
model of feto-maternal dialogue; and we performed
co-cultures of maternal and paternal PBMCs to test
VIP effects on the systemic maternal alloresponse.
After the interaction with trophoblast cells, RSA
patients displayed low frequency of CD4+CD25+
FoxP3+ cells within maternal PBMCs and low levels
of TGF-b (P < 0.05; Mann?Whitney test). VIP could
not modulate the tolerogenic response in RSA
patients as did in fertile women. However, during
the trophoblast-RSA-PBMCs dialogue, VIP could
modulate the initial inflammatory response in favor
of a Th2 pattern response evidenced by a reduction
in IL-6 and nitric oxide production while increased
IL-10 and IL-5 secretion (P < 0.05; Student t test for
each mediator). VIP effect on the cytokine-modulation
balance was also accompanied with a significant
reduction in TGF-b expression. Taken together these
results suggest that VIP, produced by trophoblast
cells under physiological conditions, favors a maternal
tolerogenic response and could normalize the exacerbated-initial inflammatory response in RSA patients.