Intravenous injection of micafungin counteracts Candida albicans-induced aggravation of duodenal ulcers caused by cysteamine in rats

Tetsuya Nakamura, Masashi Yoshida, Yuukou Kitagawa, Longxue Jin, Hideki Ishikawa, Kaori Kameyama, Go Wakabayashi, Minoru Tanabe, Shigeyuki Kawachi, Masahiro Shinoda, Yoshiro Saikawa, Norihito Wada, Tetsuro Kubota, Koichiro Kumai, Katsuko Sano, Masaki Kitajima

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)2422-2428
Number of pages7
JournalDigestive Diseases and Sciences
Volume53
Issue number9
DOIs
Publication statusPublished - 2008 Sep

Fingerprint

Cysteamine
Duodenal Ulcer
Candida albicans
Intravenous Injections
Peptic Ulcer Perforation
micafungin
Virulence Factors
Peptic Ulcer
Ulcer
Wistar Rats

Keywords

  • Antifungal drug
  • Candida
  • Cysteamine
  • Infection
  • Micafungin
  • Perforation
  • Ulcer

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Intravenous injection of micafungin counteracts Candida albicans-induced aggravation of duodenal ulcers caused by cysteamine in rats. / Nakamura, Tetsuya; Yoshida, Masashi; Kitagawa, Yuukou; Jin, Longxue; Ishikawa, Hideki; Kameyama, Kaori; Wakabayashi, Go; Tanabe, Minoru; Kawachi, Shigeyuki; Shinoda, Masahiro; Saikawa, Yoshiro; Wada, Norihito; Kubota, Tetsuro; Kumai, Koichiro; Sano, Katsuko; Kitajima, Masaki.

In: Digestive Diseases and Sciences, Vol. 53, No. 9, 09.2008, p. 2422-2428.

Research output: Contribution to journalArticle

Nakamura, T, Yoshida, M, Kitagawa, Y, Jin, L, Ishikawa, H, Kameyama, K, Wakabayashi, G, Tanabe, M, Kawachi, S, Shinoda, M, Saikawa, Y, Wada, N, Kubota, T, Kumai, K, Sano, K & Kitajima, M 2008, 'Intravenous injection of micafungin counteracts Candida albicans-induced aggravation of duodenal ulcers caused by cysteamine in rats', Digestive Diseases and Sciences, vol. 53, no. 9, pp. 2422-2428. https://doi.org/10.1007/s10620-007-0159-9
Nakamura, Tetsuya ; Yoshida, Masashi ; Kitagawa, Yuukou ; Jin, Longxue ; Ishikawa, Hideki ; Kameyama, Kaori ; Wakabayashi, Go ; Tanabe, Minoru ; Kawachi, Shigeyuki ; Shinoda, Masahiro ; Saikawa, Yoshiro ; Wada, Norihito ; Kubota, Tetsuro ; Kumai, Koichiro ; Sano, Katsuko ; Kitajima, Masaki. / Intravenous injection of micafungin counteracts Candida albicans-induced aggravation of duodenal ulcers caused by cysteamine in rats. In: Digestive Diseases and Sciences. 2008 ; Vol. 53, No. 9. pp. 2422-2428.
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abstract = "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.",
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AU - Nakamura, Tetsuya

AU - Yoshida, Masashi

AU - Kitagawa, Yuukou

AU - Jin, Longxue

AU - Ishikawa, Hideki

AU - Kameyama, Kaori

AU - Wakabayashi, Go

AU - Tanabe, Minoru

AU - Kawachi, Shigeyuki

AU - Shinoda, Masahiro

AU - Saikawa, Yoshiro

AU - Wada, Norihito

AU - Kubota, Tetsuro

AU - Kumai, Koichiro

AU - Sano, Katsuko

AU - Kitajima, Masaki

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N2 - 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.

AB - 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.

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