Objective To investigate the possible role of estrogen in the pathogenesis of vulvovaginal candidiasis（VVC）. Methods Estrogen-dependent experimental murine model of C. albicans vaginal infection was established by i...Objective To investigate the possible role of estrogen in the pathogenesis of vulvovaginal candidiasis（VVC）. Methods Estrogen-dependent experimental murine model of C. albicans vaginal infection was established by injecting subcutaneously with estradiol benzoate and then 5 × 10^6 stationary-phase C. albicans blastoconidia was inoculated intravaginally to mice （group El）, and other 3 groups were set up.＂ estrogen-treated but not infected （group E）; estrogen-untreated but infected （group I）; normal control （group C）. The dynamic change of colony-forming unit （CFU） of cervivovaginal lavage fluid was observed. Vaginal tissues at different time points （d 2, d 4, d 7 and d 14） after inoculation of C. albicans were obtained. In situ hybridization staining was used to detect expression of cyclooxygenase-2 （COX-2） mRNA and expression of nuclear factor-κB （NF-κB） was examined by immuohistochemistry. ELISA was applied to determine the interlenkin-1β （IL-1β） level. Results The constitutional high level expression of COX-2 mRNA in the vaginal tissue of group E was significantly higher than that in group C on d 4 and d 7 （P〈0. 01）, and the optical density （OD） in group EI was higher than that in the other 3 groups （P〈0.05）. There were higher IL-1β levels in vaginal tissues from d 4 to d 7 postinoculation in group EI and group I than group C （P〈0.01）. Furthermore, IL-1β in group EI was markedly elevated on d 4 and d 7 compared with group I （P〈0.01）. Compared with group C, the expression of NF-κB in group E was increased obviously on d 4 （P〈0.01）, and there was significant difference between group E1 and group I on d 4 and d 7 （P〈0.01）. Conclusions In the murine model of estrogen-dependent experimental WC, estrogen promotes the infection establishment by up-regulating expression of COX-2 via activating NF-κB signal pathway, and the high expression of COX-2 promoted by the interaction of IL-1β and NF-κB after infection formation was involved in persistence of infection.展开更多
文摘Objective To investigate the possible role of estrogen in the pathogenesis of vulvovaginal candidiasis（VVC）. Methods Estrogen-dependent experimental murine model of C. albicans vaginal infection was established by injecting subcutaneously with estradiol benzoate and then 5 × 10^6 stationary-phase C. albicans blastoconidia was inoculated intravaginally to mice （group El）, and other 3 groups were set up.＂ estrogen-treated but not infected （group E）; estrogen-untreated but infected （group I）; normal control （group C）. The dynamic change of colony-forming unit （CFU） of cervivovaginal lavage fluid was observed. Vaginal tissues at different time points （d 2, d 4, d 7 and d 14） after inoculation of C. albicans were obtained. In situ hybridization staining was used to detect expression of cyclooxygenase-2 （COX-2） mRNA and expression of nuclear factor-κB （NF-κB） was examined by immuohistochemistry. ELISA was applied to determine the interlenkin-1β （IL-1β） level. Results The constitutional high level expression of COX-2 mRNA in the vaginal tissue of group E was significantly higher than that in group C on d 4 and d 7 （P〈0. 01）, and the optical density （OD） in group EI was higher than that in the other 3 groups （P〈0.05）. There were higher IL-1β levels in vaginal tissues from d 4 to d 7 postinoculation in group EI and group I than group C （P〈0.01）. Furthermore, IL-1β in group EI was markedly elevated on d 4 and d 7 compared with group I （P〈0.01）. Compared with group C, the expression of NF-κB in group E was increased obviously on d 4 （P〈0.01）, and there was significant difference between group E1 and group I on d 4 and d 7 （P〈0.01）. Conclusions In the murine model of estrogen-dependent experimental WC, estrogen promotes the infection establishment by up-regulating expression of COX-2 via activating NF-κB signal pathway, and the high expression of COX-2 promoted by the interaction of IL-1β and NF-κB after infection formation was involved in persistence of infection.
