Immunological aspects of recurrent vaginal candidiasis [RVC] in prgnant and non pregnant patient

ABSTRACT

A possible monocyte/macrophage defect and the effect of progesterone hormone were studied in 40 cases of recurrent vaginal candidiasis [RVC], 20 pregnant and 20 non pregnant versus 20 healthy control women. Mitogen [phytohemagglutinin] induced lymphocyte proliferation and blastogenic transformation were comparable in patient and control groups. In marked contrast, Candida induced lymphocyte responses were significantly [P < 0.001] reduced in patient groups than control [36.5 +/- 3.2, for pregnant, 45 +/- 4.2 for non pregnant and 87.5 +/- 4.3 for controls]. In vitro depletion of patients' monocytes [adherent cell population] from whole peripheral blood' mononuclear layer [PBML], improved the lymphocyte responses [P < 0.001] suggesting a down regulatory role of patients' macrophages on the immune response to Candida in cases of RVC. A trial was made to correct this macrophagal dysfunction by in vitro addition of prostaglandin inhibitors [indomethacin 4 umol/L] to cell cultures. Significant [P < 0.001] improvement in Iymphocyte responses were noticed suggesting that this macrophagal defect may be attributed to abnormal excess production of prostaglandins. When progesterone hormone was added in vitro to cell cultures with concentrations equivalent to its level observed in the menstrual cycle [0.15 ng/ml in proliferative phase and 25 ng/ml ID luteal phase] a significant [P < 0.001] inhibition in lymphocyte responses were obtained in the presence of luteal phase level. In vitro depletion of monocytes masked this inhibitory effect, suggesting that the progesterone hormone inhibits the immune response to Candida via monocyte ependent mechanism. We concluded that fluctuations in a woman's macrophagal activity in cases of RVC may account for the frequent recurrent attacks of such disease. This macrophagal defect may be predisposed by high levels of progesterone hormone, which may suggest a type of receptors for progesterone on monocytes, and corrected by incorporation of prostaglandin inhibitors in the treatment