Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
J Diabetes Res 2014
PMID:A novel diabetic murine model of Candida albicans-induced mucosal inflammation and proliferation. 2469 42

Chronic hyperplastic candidiasis progresses from squamous cell hyperplasia to squamous cell carcinoma (SCC); however, the oncogenic mechanism remains unclear. In the present study, we attempted to induce opportunistic Candida albicans infection and establish chronic hyperplastic candidiasis in rats by combining diabetic condition and prednisolone administration, followed by analysis of the inflammatory cells involved in the disease progression. Female Wistar Bunn/Kobori (WBN/Kob) rats were divided into 3 groups: alloxan-induced diabetic rats (A group) along with diabetic (AP group) and nondiabetic (P group) rats intermittently treated with prednisolone. Animals were euthanized at 42 weeks of age. Squamous cell hyperplasia following C. albicans infection in the forestomach was observed in almost all AP and A group rats. The lesions in the AP group were significantly more severe than those in the A group. In addition, SCC was detected in 1 AP group animal. Cluster of differentiation (CD)4-positive T cell and CD68-positive macrophage infiltration in the AP group was significantly stronger than that in the A group. These findings suggest that the combination of diabetes and intermittent prednisolone administration could induce chronic hyperplastic candidiasis without direct C. albicans inoculation and that CD4-positive T cells and CD68-positive macrophages may be highly involved in the pathogenesis of these hyperplastic lesions.
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PMID:Induction of Severe Chronic Hyperplastic Candidiasis in Rat by Opportunistic Infection of C. albicans through Combination of Diabetes and Intermittent Prednisolone Administration. 2883 Mar 1