title: Candida albicans aggravates duodenal ulcer perforation induced by administration of cysteamine in rats.
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 10(8) 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 mm2, whereas that in the saline group was 16.53 +/- 20.4 mm2 (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.
  
  
  CONCLUSIONS
  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.
authors: Department of Surgery, Keio University School of Medicine, Tokyo, Japan.
authors: Tetsuya
authors: T
authors: Nakamura
authors: Masashi
authors: M
authors: Yoshida
authors: Hideki
authors: H
authors: Ishikawa
authors: Kaori
authors: K
authors: Kameyama
authors: Go
authors: G
authors: Wakabayashi
authors: Yoshihide
authors: Y
authors: Otani
authors: Motohide
authors: M
authors: Shimazu
authors: Minoru
authors: M
authors: Tanabe
authors: Shigeyuki
authors: S
authors: Kawachi
authors: Koichiro
authors: K
authors: Kumai
authors: Tetsuro
authors: T
authors: Kubota
authors: Yoshiro
authors: Y
authors: Saikawa
authors: Katsuko
authors: K
authors: Sano
authors: Masaki
authors: M
authors: Kitajima
mesh_terms: D000818:Animals; D016282:Aspartic Acid Endopeptidases / Q000378:metabolism; D002176:Candida albicans / Q000201:enzymology / Q000302:isolation & purification*; D002177:Candidiasis / Q000150:complications* / Q000201:enzymology / Q000382:microbiology / Q000473:pathology; D003543:Cysteamine; D004381:Duodenal Ulcer / Q000139:chemically induced / Q000150:complications* / Q000201:enzymology / Q000473:pathology; D004386:Duodenum / Q000201:enzymology / Q000382:microbiology* / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000382:microbiology; D006098:Granulocytes / Q000382:microbiology; D007150:Immunohistochemistry; D008297:Male; D010439:Peptic Ulcer Perforation / Q000201:enzymology / Q000209:etiology* / Q000382:microbiology / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D003543:Cysteamine; D016282:Aspartic Acid Endopeptidases