Candida albicans aggravates duodenal ulcer perforation induced by administration of cysteamine in rats

Tetsuya Nakamura, Masashi Yoshida, Hideki Ishikawa, Kaori Kameyama, Go Wakabayashi, Yoshihide Otani, Motohide Shimazu, Minoru Tanabe, Shigeyuki Kawachi, Koichiro Kumai, Tetsuro Kubota, Yoshiro Saikawa, Katsuko Sano, Masaki Kitajima

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Background: Candida sp are frequently isolated from the ascitic fluid of patients with perforated ulcers. The present study was performed to examine whether Candida infection may be involved in the process of ulcer perforation. Methods: Male Wistar rats were divided into a saline group (n = 15) and a Candida group (n = 17). Cysteamine-HCl (Sigma; 31 mg/100 g) was administered thrice on day 1 to both groups of animals. Candida albicans at a density of 108 in 0.5 mL of saline was administered 1 h before, and 12 h and 24 h after the first administration of cysteamine in the Candida group. Results: Perforated duodenal ulcers were observed in 94.1% of the rats in the Candida group, but only 26.7% of the rats in the saline group (P < 0.01). The area of the duodenal ulcers in the Candida group was 40.89 ± 33.07 mm 2, whereas that in the saline group was 16.53 ± 20.4 mm 2 (P < 0.05). The mortality rate was significantly higher in the Candida group than in the saline group. In the Candida group, colonization by C. albicans was recognized at the ulcer base, surrounded by marked granulocytic infiltration. The number of eosinophils infiltrating the ulcer base was also significantly greater in the Candida group than in the saline group. Immunohistochemical analysis revealed the expression of secretory aspartyl protease (SAP) in the region of the ulcer showing colonization by C. albicans in the Candida group. Conclusion: Candida albicans aggravates duodenal ulcer perforation in the experimental model of cysteamine-induced duodenal ulcer perforation. The present findings suggest that SAP and host-parasite relationships, including granulocyte-dependent mechanisms, may be involved in the aggravation of ulcer perforation by C. albicans.

Original languageEnglish
Pages (from-to)749-756
Number of pages8
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume22
Issue number5
DOIs
Publication statusPublished - 2007

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Cysteamine
Duodenal Ulcer
Candida albicans
Candida
Ulcer
Aspartic Acid Proteases
Host-Parasite Interactions
Ascitic Fluid
Granulocytes
Eosinophils
Wistar Rats
Theoretical Models

Keywords

  • Eosinophil
  • Helicobacter pylori
  • Infection
  • Secretory aspartyl protease
  • Stomach

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

Candida albicans aggravates duodenal ulcer perforation induced by administration of cysteamine in rats. / Nakamura, Tetsuya; Yoshida, Masashi; Ishikawa, Hideki; Kameyama, Kaori; Wakabayashi, Go; Otani, Yoshihide; Shimazu, Motohide; Tanabe, Minoru; Kawachi, Shigeyuki; Kumai, Koichiro; Kubota, Tetsuro; Saikawa, Yoshiro; Sano, Katsuko; Kitajima, Masaki.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 22, No. 5, 2007, p. 749-756.

Research output: Contribution to journalArticle

Nakamura, T, Yoshida, M, Ishikawa, H, Kameyama, K, Wakabayashi, G, Otani, Y, Shimazu, M, Tanabe, M, Kawachi, S, Kumai, K, Kubota, T, Saikawa, Y, Sano, K & Kitajima, M 2007, 'Candida albicans aggravates duodenal ulcer perforation induced by administration of cysteamine in rats', Journal of Gastroenterology and Hepatology (Australia), vol. 22, no. 5, pp. 749-756. https://doi.org/10.1111/j.1440-1746.2006.04353.x
Nakamura, Tetsuya ; Yoshida, Masashi ; Ishikawa, Hideki ; Kameyama, Kaori ; Wakabayashi, Go ; Otani, Yoshihide ; Shimazu, Motohide ; Tanabe, Minoru ; Kawachi, Shigeyuki ; Kumai, Koichiro ; Kubota, Tetsuro ; Saikawa, Yoshiro ; Sano, Katsuko ; Kitajima, Masaki. / Candida albicans aggravates duodenal ulcer perforation induced by administration of cysteamine in rats. In: Journal of Gastroenterology and Hepatology (Australia). 2007 ; Vol. 22, No. 5. pp. 749-756.
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abstract = "Background: Candida sp are frequently isolated from the ascitic fluid of patients with perforated ulcers. The present study was performed to examine whether Candida infection may be involved in the process of ulcer perforation. Methods: Male Wistar rats were divided into a saline group (n = 15) and a Candida group (n = 17). Cysteamine-HCl (Sigma; 31 mg/100 g) was administered thrice on day 1 to both groups of animals. Candida albicans at a density of 108 in 0.5 mL of saline was administered 1 h before, and 12 h and 24 h after the first administration of cysteamine in the Candida group. Results: Perforated duodenal ulcers were observed in 94.1{\%} of the rats in the Candida group, but only 26.7{\%} of the rats in the saline group (P < 0.01). The area of the duodenal ulcers in the Candida group was 40.89 ± 33.07 mm 2, whereas that in the saline group was 16.53 ± 20.4 mm 2 (P < 0.05). The mortality rate was significantly higher in the Candida group than in the saline group. In the Candida group, colonization by C. albicans was recognized at the ulcer base, surrounded by marked granulocytic infiltration. The number of eosinophils infiltrating the ulcer base was also significantly greater in the Candida group than in the saline group. Immunohistochemical analysis revealed the expression of secretory aspartyl protease (SAP) in the region of the ulcer showing colonization by C. albicans in the Candida group. Conclusion: Candida albicans aggravates duodenal ulcer perforation in the experimental model of cysteamine-induced duodenal ulcer perforation. The present findings suggest that SAP and host-parasite relationships, including granulocyte-dependent mechanisms, may be involved in the aggravation of ulcer perforation by C. albicans.",
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T1 - Candida albicans aggravates duodenal ulcer perforation induced by administration of cysteamine in rats

AU - Nakamura, Tetsuya

AU - Yoshida, Masashi

AU - Ishikawa, Hideki

AU - Kameyama, Kaori

AU - Wakabayashi, Go

AU - Otani, Yoshihide

AU - Shimazu, Motohide

AU - Tanabe, Minoru

AU - Kawachi, Shigeyuki

AU - Kumai, Koichiro

AU - Kubota, Tetsuro

AU - Saikawa, Yoshiro

AU - Sano, Katsuko

AU - Kitajima, Masaki

PY - 2007

Y1 - 2007

N2 - Background: Candida sp are frequently isolated from the ascitic fluid of patients with perforated ulcers. The present study was performed to examine whether Candida infection may be involved in the process of ulcer perforation. Methods: Male Wistar rats were divided into a saline group (n = 15) and a Candida group (n = 17). Cysteamine-HCl (Sigma; 31 mg/100 g) was administered thrice on day 1 to both groups of animals. Candida albicans at a density of 108 in 0.5 mL of saline was administered 1 h before, and 12 h and 24 h after the first administration of cysteamine in the Candida group. Results: Perforated duodenal ulcers were observed in 94.1% of the rats in the Candida group, but only 26.7% of the rats in the saline group (P < 0.01). The area of the duodenal ulcers in the Candida group was 40.89 ± 33.07 mm 2, whereas that in the saline group was 16.53 ± 20.4 mm 2 (P < 0.05). The mortality rate was significantly higher in the Candida group than in the saline group. In the Candida group, colonization by C. albicans was recognized at the ulcer base, surrounded by marked granulocytic infiltration. The number of eosinophils infiltrating the ulcer base was also significantly greater in the Candida group than in the saline group. Immunohistochemical analysis revealed the expression of secretory aspartyl protease (SAP) in the region of the ulcer showing colonization by C. albicans in the Candida group. Conclusion: Candida albicans aggravates duodenal ulcer perforation in the experimental model of cysteamine-induced duodenal ulcer perforation. The present findings suggest that SAP and host-parasite relationships, including granulocyte-dependent mechanisms, may be involved in the aggravation of ulcer perforation by C. albicans.

AB - Background: Candida sp are frequently isolated from the ascitic fluid of patients with perforated ulcers. The present study was performed to examine whether Candida infection may be involved in the process of ulcer perforation. Methods: Male Wistar rats were divided into a saline group (n = 15) and a Candida group (n = 17). Cysteamine-HCl (Sigma; 31 mg/100 g) was administered thrice on day 1 to both groups of animals. Candida albicans at a density of 108 in 0.5 mL of saline was administered 1 h before, and 12 h and 24 h after the first administration of cysteamine in the Candida group. Results: Perforated duodenal ulcers were observed in 94.1% of the rats in the Candida group, but only 26.7% of the rats in the saline group (P < 0.01). The area of the duodenal ulcers in the Candida group was 40.89 ± 33.07 mm 2, whereas that in the saline group was 16.53 ± 20.4 mm 2 (P < 0.05). The mortality rate was significantly higher in the Candida group than in the saline group. In the Candida group, colonization by C. albicans was recognized at the ulcer base, surrounded by marked granulocytic infiltration. The number of eosinophils infiltrating the ulcer base was also significantly greater in the Candida group than in the saline group. Immunohistochemical analysis revealed the expression of secretory aspartyl protease (SAP) in the region of the ulcer showing colonization by C. albicans in the Candida group. Conclusion: Candida albicans aggravates duodenal ulcer perforation in the experimental model of cysteamine-induced duodenal ulcer perforation. The present findings suggest that SAP and host-parasite relationships, including granulocyte-dependent mechanisms, may be involved in the aggravation of ulcer perforation by C. albicans.

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KW - Helicobacter pylori

KW - Infection

KW - Secretory aspartyl protease

KW - Stomach

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