IMMUNMODULATING CYTOKINES INDUCE TERM AND PRETERM PARTURITION

The aim of our study was to investigate if cytokines, which are able t o cause preterm delivery in case of intraamniotic infection, also part icipate in the mechanisms of normal term labor. Therefore we estimated cytokine concentrations in cercicovaginal secretions of 96 patients, divided into four different collectives. In collective A (women with s pontaneous term labor) cytokine concentrations raised from a median le vel of 278 pg/ml for Il-1 beta and 263 pg/ml for Il-6 in early term la bor to a median level of 3351 pg/ml for Il-1 beta and 39442 pg/ml for Il-6 at complete cervical dilatation. TNF-alpha-exclusively appeared a fter spontaneous rupture of fetal membranes. In collective B and C (wo men with preterm rupture of fetal membranes) cytokine concentrations d eclined from a maximum level of 1425 pg/ml for TNF-alpha, 12982 pg/ml for Il-1 beta and 29727 pg/ml for Il-6 soon after preterm rupture of m embranes to a minimum level of 93 pg/ml for TNF-alpha, 851 pg/ml for I l-1 beta and 780 pg/ml for Il-6 with remission of labor in case of suc cessful tocolytic treatment. High concentrations reappeared with the o nset of labor, unresponsive to tocolysis. In collective D (women with intact membranes) TNF-alpha was not detectable and Il-1 beta and Il-6 appeared exclusively in the presence of labor. Our results suggest, th at normal term labor may be controlled by biochemical processes, simil ar to infection-associated signal transduction, which is commonly acce pted to induce preterm labor.