title: A novel diabetic murine model of Candida albicans-induced mucosal inflammation and proliferation.
abstract: Chronic hyperplastic candidiasis (CHC) lesions will progress to dysplasia with some of these developing squamous cell carcinoma (SCC). It is well known that diabetic patients are predisposed to candidiasis. Previously, we found that alloxan-induced diabetic rats spontaneously have mucosal hyperplasia with C. albicans infection and that those lesions progress to SCC. Here, we developed a rat model of candidiasis with diabetes progressing to mucosal proliferation. Diabetes was induced in thirty rats by single intravenous administration of alloxan. Ten nondiabetic rats and fifteen diabetic rats then received C. albicans containing solution orally, and additional fifteen diabetic rats received saline in the same manner. The administration of C. albicans induced mucosal candidiasis and the related mucosal hyperplastic changes in all the diabetic rats and progressed to SCC in one rat. Chronic suppurative inflammation of the mucosa developed in the forestomach with infection by C. albicans. The same lesions were only detected in the forestomach of 4 diabetic rats without C. albicans treatment. After C. albicans treatment, none of the nondiabetic rats showed mucosal changes or fungus infection in the forestomach. These findings demonstrate that a prolonged diabetic condition can cause C. albicans infection and enhance C. albicans-related mucosal hyperplasia.
authors.affiliation: Department of Pathology, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata, Osaka 573-0101, Japan.
authors.forename: Tomoya
authors.initials: T
authors.lastname: Sano
authors.affiliation: Department of Pathology, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata, Osaka 573-0101, Japan.
authors.forename: Kiyokazu
authors.initials: K
authors.lastname: Ozaki
authors.affiliation: Department of Pathology, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata, Osaka 573-0101, Japan.
authors.forename: Yui
authors.initials: Y
authors.lastname: Terayama
authors.affiliation: Laboratory of Clinicopathological Therapeutics, Faculty of Pharmaceutical Sciences, Hiroshima International University, Kure, Hiroshima 737-0112, Japan.
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Kodama
authors.affiliation: Department of Pathology, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata, Osaka 573-0101, Japan.
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Matsuura
mesh_terms: D000496:Alloxan; D000818:Animals; D002176:Candida albicans / Q000254:growth & development / Q000276:immunology / Q000472:pathogenicity* / Q000502:physiology; D002177:Candidiasis / Q000150:complications* / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D002294:Carcinoma, Squamous Cell / Q000209:etiology / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000276:immunology; D048909:Diabetes Complications / Q000276:immunology / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000150:complications; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D005756:Gastritis / Q000150:complications* / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D054884:Host-Pathogen Interactions; D006965:Hyperplasia; D018928:Immunity, Mucosal; D051381:Rats; D011922:Rats, Mutant Strains; D013047:Specific Pathogen-Free Organisms; D013270:Stomach / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D013274:Stomach Neoplasms / Q000209:etiology / Q000276:immunology / Q000382:microbiology / Q000473:pathology
chemical_list: D000496:Alloxan