MOLECULAR MECHANISMS INVOLVED IN THE DIFFERENTIAL EFFECTS OF SEX STEROIDS ON THE REPRODUCTION AND INFECTIVITY OF TAENIA CRASSICEPS

The in vitro exposure of Taenia crassiceps cysticerci to 17-β estradiol (E₂) and progesterone (P₄) stimulated their reproduction and infectivity. Testosterone (T₄) and dihydrotestosterone (DHT) inhibited their reproduction and reduced their motility and infectivity. E₂ and P₄ increased, whereas T₄ and DHT reduced, the expression of parasite c-fos and c-jun and DNA synthesis. In vitro exposure of cysticerci to sex steroids before their inoculation into recipient noninfected mice resulted in large parasite loads when pretreated with E₂ and P₄ and in smaller loads when pretreated with T₄ and DHT. To determine the possible molecular mechanisms by which sex steroids affect T. crassiceps, sex steroid receptors were amplified. Taenia crassiceps expressed estrogen receptors (both α and β isoforms) and androgen receptors but no P₄ receptors. These results demonstrate that sex steroids act directly on parasite reproduction by binding to a classic and specific sex steroid receptor on the parasite. The differential response of cysticerci to sex steroids may also be involved in their ability to grow faster in the murine female or feminized male host. This is the first report of direct sex steroid effects on the parasite possibly through sex steroid receptors in the cysticerci.