Candida albicans aggravates duodenal ulcer perforation induced by administration of cysteamine in rats.
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.
Nakamura
Tetsuya
T
Department of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yoshida
Masashi
M
Ishikawa
Hideki
H
Kameyama
Kaori
K
Wakabayashi
Go
G
Otani
Yoshihide
Y
Shimazu
Motohide
M
Tanabe
Minoru
M
Kawachi
Shigeyuki
S
Kumai
Koichiro
K
Kubota
Tetsuro
T
Saikawa
Yoshiro
Y
Sano
Katsuko
K
Kitajima
Masaki
M
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
D003543:Cysteamine; D016282:Aspartic Acid Endopeptidases