The purpose of this study is to determine the effect of labor on the placental cytokine production. Certain cytokines, specifically TNFα, can serve as an autocrine growth factor for HIV replication by directly activating the NF-κB site on the HIV promotor area, increasing viral transcription. We hypothesized that labor may change the cytokines profile that are produced locally in the placenta favoring HIV vertical transmission. We studied the placental production of TNFα, IL1α, IL2, IL4, IL6, IL8 and IL10 by culturing non-infected placental tissue for 24 hours (0.2gm of wet tissue/ml media). Cytokine levels were measured in the supernatant using enzyme immunoassay. Term placental tissue obtained after labor produced a significant large amount of TNFα, IL1α and IL10 compared to placental tissue obtained before labor (Fig., mean ± SD). There was no difference in the placental production of IL6 and IL8 in relation to labor, whereas IL2 and IL4 could not be detected either before or after labor. The placental production of TNFα, before labor, in first trimester placentas (12.3 ± 6.2 pg/ml, mean ± SD) was compared to third trimester placentas (9.2 ± 2.2 pg/ml, mean± SD) with no significant difference (P = NS). We concluded that, labor increases placental production of TNFα, IL1α and IL10 with no effect on IL6 or IL8. We speculate that at the time of labor there is increased production of different cytokines, namely TNFα, that may increase the risk of HIV transmission from a mother to her infant.

figure 1

Figure 1

This work was supported by NIH Grant CA 55910 (S.S.)