15-HYDROXYPROSTAGLANDIN DEHYDROGENASE - IMPLICATIONS IN PRETERM LABORWITH AND WITHOUT ASCENDING INFECTION

There is evidence that intrauterine infection, which stimulates PG syn thesis may play a role in the pathogenesis of some preterm labor. Loca l tissue concentrations of PGs are controlled not only by the rate of synthesis, but also by catabolism, which is regulated by 15-hydroxypro staglandin dehydrogenase (PGDH). We hypothesized that a decrease of PG DH activity could contribute to an increase in PG output at the time o f preterm labor (PTL) especially in association with infection. We mea sured PGDH activity with a zero order kinetic enzymatic assay, PGDH me ssenger ribonucleic acid by in situ hybridization and PGDH distributio n and localization with immunohistochemistry in human placenta and fet al membranes from women at term before (n = 10) or after (n = 16) labo r compared to preterm labor at less than 36 weeks without (n = 16) and with (n = 11) chorioamnionitis. PGDH activity in chorion was signific antly lower in PTL than at term and was further reduced when PTL was a ssociated with inflammation. Immunoreactive PGDH and PGDH messenger ri bonucleic acid localized predominantly to chorionic trophoblasts at te rm and were reduced in PTL women with or without infection. These effe cts were not observed in the placenta. Loss of PGDH with infection was associated with infiltration of chorion by polymorphonuclear leukocyt es, resulting in a compromised structural integrity, although the amni otic epithelium was generally intact. We conclude that a reduction in PGDH in the human fetal membranes may occur in some cases of preterm l abor and may contribute to an increase in net PG accumulation and driv e to myometrial contractility.