Immunoreactive 15-hydroxyprostaglandin dehydrogenase (PGDH) is reduced in fetal membranes from patients at preterm delivery in the presence of infection.

Previously we reported that the proportion of trophoblast cells that were immunopositive for 15-OH prostaglandin dehydrogenase (PGDH) in the chorionic membranes was reduced in women in preterm labour without infection, compared with women at term, but was not altered in preterm labour patients with an underlying infective process. Subsequently, we found that PGDH activity and PGDH mRNA were significantly lower in membranes of this latter group of patients than in women at preterm labour without infection or at term. To resolve this issue we used immunohistochemistry to examine the distribution and frequency of immunoreactive (ir)-PGDH positive cells in full-thickness fetal membranes in patients at preterm labour in the presence or absence of infection. Trophoblast and decidual stromal cells were identified using antibodies against cytokeratin and vimentin, respectively. There was considerable variation in the number of chorionic trophoblast cells that were positive for ir-PGDH, but in some patients there was little or no ir-PGDH staining, and this was associated with loss of trophoblast cells from the tissue. The mean intensity and number of ir-PGDH positive cells was significantly lower in membranes from patients in preterm labour with infection than in idiopathic preterm labour at which the diagnosis of infection was not made. We conclude that in the setting of preterm labour with infection there may be loss of trophoblast cells from membranes, with corresponding reduction in the number of ir-PGDH positive cells. Loss of PGDH activity removes the initial step in activating primary prostaglandins, which are then able to pass unmetabolized to the decidua and myometrium, and contribute to the stimulus to preterm birth.