Objectives: There is growing evidence that Th1/Th2 imbalance in cytokine network may play role in immunopathology of preeclampsia (PE). Normal pregnancy is "Th2 phenomenon" while PE is believed to be caused by Th1-shift. There is few data concerning Th1/Th2 imbalance in transient hypertension of pregnancy (TH).
Design: The aim of this study was to check the hypothesis that changes in IFN-gamma and IL-2 (Th1 cytokines) levels are accompanied with deficit in TGF-beta (anti-Th1 cytokine) production in TH.
Materials and methods: The study group consisted of 10 pregnant women with TH diagnosed between 30-37 week of gestation (mean age 27.0 +/- 3.0 years, mean gestational age 33.5 +/- 3.0 weeks) and 10 women with uncomplicated pregnancy (mean age 26.0 +/- 3.5 years, mean gestational age 35.5 +/- 1.5 weeks). All women were primigravidae matched according to gestational age and race. They had no diabetes mellitus and renal diseases prior to pregnancy neither had any features of them during the study. They had no hypertension before pregnancy. Exclusion criteria were: uterine contractions, infection and therapy with steroids before blood sampling. TH was defined according to USA National Health Institute criteria. Peripheral blood lymphocytes (PBL) were cultured for 72 hours in standard 1640 RPMI medium enriched with 20% FCS, L-glutamine, antibiotics (Sigma) and mitogen phytohemaglutynine (PHA) (Sigma). Cytokine levels were estimated in culture supernatants by using standard ELISA kits according to the indications of the producer (R&D). Statistical analysis was performed with Student-T test.
Results: In TH group the levels of IL-2 were higher compared with control group but the differences did not reach statistical significance (4.5 vs. 1.56 pg/ml, t = -1.00, p < 0.1). The same referred to IFN-gamma levels (754.0 vs. 771.0 pg/ml, t = -0.04, NS). However, TGF-beta levels were significantly lower in TH group compared with control group (2459.2 vs. 4156.4 pg/ml, t = -1.47, p < 0.05). Conclusion is that there is a significant deficit of TGF-beta production in peripheral blood lymphocytes of women with TH studied "in vitro". This may contribute to Th1-shift seen in TH similarly to PE.