A macrophage defect in women with recurrent Candida vaginitis and its reversal in vitro by prostaglandin inhibitors.
The possible involvement of a defect in cellular immunity in the etiology of recurrent vaginal candidiasis was explored. The mean and range of in vitro lymphocyte proliferative responses induced by mitogens were comparable in 65 patients and 36 control subjects. In contrast, Candida-directed proliferation was reduced at least 70% below the mean control value in 73% of the patients. Further analyses on selected patients demonstrated that lymphocytes of the patients responded in the normal range to Candida if incubated in the presence of control macrophages. Conversely, macrophages of patients inhibited the responses of control lymphocytes to Candida. These effects were independent of mixed leukocyte reactions between allogeneic cells. Addition of the prostaglandin inhibitors ibuprofen and indomethacin prevented macrophages of patients from inhibiting patient or control lymphocyte proliferation. In response to Candida, macrophages from some women with recurrent vaginitis produce prostaglandin, which blocks the lymphocyte proliferation response to this organism.
D002181:Candidiasis, Vulvovaginal / Q000276:immunology*; D002448:Cell Adhesion / Q000187:drug effects; D005260:Female; D006801:Humans; D007052:Ibuprofen / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000187:drug effects; D007959:Lymphocyte Culture Test, Mixed; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D009637:Masoprocol / Q000494:pharmacology; D008934:Mitogens / Q000494:pharmacology; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D012008:Recurrence
D008934:Mitogens; D011448:Prostaglandin Antagonists; D009637:Masoprocol; D007052:Ibuprofen; D007213:Indomethacin