CONICET | Buscador de Institutos y Recursos Humanos

p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0cm 0cm 0.0001pt; font-size: 10pt; font-family: "Times New Roman"; }div.Section1 { page: Section1; } Infection associated with Shiga toxin-producing Escherichia coli (STEC) and subsequent Hemolytic-Uremic Syndrome (HUS) became relevant in public health since it was considered as one of the most important emergent pathogens. The major virulence factor of STEC is Shiga toxin type 1 or 2 (Stx1, Stx2). Shiga toxin-producing Escherichia coli (STEC) infections could be one of the causes of fetal morbimortality in pregnant women. We had reported that rats in the late stage of pregnancy treated with Stx2 induced premature delivery of dead fetuses. Our previous results suggest that nitric oxide (NO) is partially involved in these mechanisms, since aminoguanidine, an iNOS specific inhibitor, blocks the effects of Stx2 on rat pregnancy. Objective Our aim was to evaluate the role of prostaglandins (PGs) in the mechanisms by which Stx2 induced preterm delivery. Materials and methods Pregnant rats on days 14-16 of gestation were i.p. injected with culture supernatant from recombinant E. coli containing 0.4 µg/ml Stx2 and 30 ng/ml LPS (sStx2). PGE and PGF2α levels were evaluated by radioimmunoassay analyses in deciduas and placentas from treated rats killed 12 h post sStx2 injection. Results Injection of sStx2 induced preterm delivery of live fetuses and dead fetuses depending on the toxin concentration. PGs production was detectable in deciduas and placenta from control animals. Stx2 increased the PGs levels in both tissues of treated rats in a dose dependent manner 12 h post-injection (p<0.05). Conclusions Our results suggest that the increased of PGs could be modulated by the increased of iNOS activity observed in these experimental conditions. Further experiments could be necessary to clarify if PGs play a central role in Stx2-induced preterm delivery.

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