BACKGROUND: We have reported previously that Candida albicans is involved in the pathogenesis of peptic ulcer perforation; it was shown that C. albicans aggravated the severity of duodenal ulceration and increased the rate of perforation. We considered it incumbent upon us to ascertain whether C. albicans is a virulence factor involved in peptic ulcer perforation. In the present study, we administered an antifungal drug (micafungin) intravenously to rats that had received intragastric (i.g.) administration of C. albicans and cysteamine, in order to examine that micafungin could counteract the C. albicans-aggravation of duodenal ulcers. METHODS: Cysteamine was administered thrice on day 1 to male Wistar rats. C. albicans was administered to the animals 1 h before, and 12 and 24 h after the first administration of cysteamine. Micafungin (n = 22) or saline (n = 24) was administered 12, 24, and 48 h after the administration of cysteamine. RESULTS: The area of the duodenal ulcers was also significantly smaller in the micafungin group (P < 0.05). In addition, the survival rate of the rats was significantly higher in the micafungin group (P < 0.05). While in the control group, the ulcer base was found to be colonized by C. albicans, there was no evidence of the presence of C. albicans in the micafungin group. CONCLUSION: It was shown that intravenous injection of micafungin counteracted the aggravation by C. albicans of cysteamine-induced duodenal ulcers in rats. This finding supports the concept that C. albicans is an aggravating factor for peptic ulcers.
BACKGROUND: We have reported previously that Candida albicans is involved in the pathogenesis of peptic ulcer perforation; it was shown that C. albicans aggravated the severity of duodenal ulceration and increased the rate of perforation. We considered it incumbent upon us to ascertain whether C. albicans is a virulence factor involved in peptic ulcer perforation. In the present study, we administered an antifungal drug (micafungin) intravenously to rats that had received intragastric (i.g.) administration of C. albicans and cysteamine, in order to examine that micafungin could counteract the C. albicans-aggravation of duodenal ulcers. METHODS:Cysteamine was administered thrice on day 1 to male Wistar rats. C. albicans was administered to the animals 1 h before, and 12 and 24 h after the first administration of cysteamine. Micafungin (n = 22) or saline (n = 24) was administered 12, 24, and 48 h after the administration of cysteamine. RESULTS: The area of the duodenal ulcers was also significantly smaller in the micafungin group (P < 0.05). In addition, the survival rate of the rats was significantly higher in the micafungin group (P < 0.05). While in the control group, the ulcer base was found to be colonized by C. albicans, there was no evidence of the presence of C. albicans in the micafungin group. CONCLUSION: It was shown that intravenous injection of micafungin counteracted the aggravation by C. albicans of cysteamine-induced duodenal ulcers in rats. This finding supports the concept that C. albicans is an aggravating factor for peptic ulcers.
Authors: L Ostrosky-Zeichner; D Kontoyiannis; J Raffalli; K M Mullane; J Vazquez; E J Anaissie; J Lipton; P Jacobs; J H Jansen van Rensburg; J H Rex; W Lau; D Facklam; D N Buell Journal: Eur J Clin Microbiol Infect Dis Date: 2005-10 Impact factor: 3.267
Authors: S Tawara; F Ikeda; K Maki; Y Morishita; K Otomo; N Teratani; T Goto; M Tomishima; H Ohki; A Yamada; K Kawabata; H Takasugi; K Sakane; H Tanaka; F Matsumoto; S Kuwahara Journal: Antimicrob Agents Chemother Date: 2000-01 Impact factor: 5.191