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The aim of our study was to investigate if cytokines, which are able to cause preterm delivery is case of intraamniotic infection, also participate 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 spontaneous term labor) cytokine concentrations raised from a median level of 278 pg/ml for Il-1 beta and 263 pg/ml for Il-6 in early term labor to a median level of 3351 pg/ml for Il-1 beta and 39,442 pg/ml for Il-6 at complete cervical dilatation. TNF-alpha-exclusively appeared after spontaneous rupture of fetal membranes. In collective B and C (women with preterm rupture of fetal membranes) cytokine concentrations declined from a maximum level of 1425 pg/ml for TNF-alpha, 12,982 pg/ml for Il-1 beta and 29,727 pg/ml for Il-6 soon after preterm rupture of membranes to a minimum level of 93 pg/ml for TNF-alpha, 851 pg/ml for Il-1 beta and 780 pg/ml for Il-6 with remission of labor in case of successful tocolytic treatment. High concentrations reappeared with the onset of labor, unresponsive to tocolysis. In collective D (women with intact membranes) TNF-alpha was not detectable and Il-1 beta and II-6 appeared exclusively in the presence of labor. Our results suggest, that normal term labor may be controlled by biochemical processes, similar to infection-associated signal transduction, which is commonly accepted to induce preterm labor.

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