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      A Novel Diabetic Murine Model of Candida albicans-Induced Mucosal Inflammation and Proliferation

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          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.

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          The microflora associated with human oral carcinomas.

          K.N. Nagy, I Sonkodi, I Szöke … (1998)
          Both local and systemic infections may complicate the morbidity of patients with oral malignant neoplasms, particularly those presenting intraorally. This study investigated the microbial contents of the biofilms present on the surfaces of oral squamous cell carcinomas. Biofilm samples were obtained from the central surface of the lesions in 21 patients (20 male, 1 female) aged 52.8 (+/- 8.2) years, and from contiguous healthy mucosa, before any antibiotic therapy or any tumour treatment. All lesions were keratinising squamous cell carcinomas with surface ulceration. Samples were transported in reduced brain heart infusion (BHI) broth and cultured within 1 h of removal, using aerobic and anaerobic complete and selective media. The median number of anaerobic colony forming units (CFU/ml) at the tumour sites (1.6 x 10(8)) was significantly higher than for the healthy (control) mucosa (3.0 x 10(7); P = 0.0001, Wilcoxon); the same was true for aerobes at the tumour sites (1.51 x 10(8)) relative to the controls (2.8 x 10(7); P = 0.0008, Wilcoxon). The species isolated in increased numbers at tumour sites were Veillonella, Fusobacterium, Prevotella, Porphyromonas, Actinomyces and Clostridium (anaerobes), and Haemophilus, Enterobacteriaceae and Streptococcus spp. (aerobes). Candida albicans was found at eight of the 21 tumour sites, but never at control sites. It was concluded that human oral carcinoma surface biofilms harbour significantly increased numbers of aerobes and anaerobes as compared with the healthy mucosal surface of the same patient. Candida albicans can also be present in these biofilms. These findings must be considered in relation to the known predisposition of such patients to systemic infections, and to the unpleasant complications of oral morbidity due to infected lesions.
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            Animal models of mucosal Candida infection.

            F Odds, Julian Naglik, Paul Fidel (2008)
            Rodent models of oral, vaginal and gastrointestinal Candida infection are described and discussed in terms of their scientific merits. The common feature of all experimental mucosal Candida infections is the need for some level of host immunocompromise or exogenous treatment to ensure quantitatively reproducible disease. A growing literature describes the contributions of such candidiasis models to our understanding of certain aspects of fungal virulence and host response to mucosal Candida albicans challenge. Evidence to date shows that T-lymphocyte responses dominate host immune defences to oral and gastrointestinal challenge, while other, highly compartmentalized responses defend vaginal surfaces. By contrast the study of C. albicans virulence factors in mucosal infection models has only begun to unravel the complex of attributes required to define the difference between strongly and weakly muco-invasive strains.
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              Experimental oral candidiasis in animal models.

              L Samaranayake, Y Samaranayake (2001)
              Oral candidiasis is as much the final outcome of the vulnerability of the host as of the virulence of the invading organism. We review here the extensive literature on animal experiments mainly appertaining to the host predisposing factors that initiate and perpetuate these infections. The monkey, rat, and mouse are the choice models for investigating oral candidiasis, but comparisons between the same or different models appear difficult, because of variables such as the study design, the number of animals used, their diet, the differences in Candida strains, and the duration of the studies. These variables notwithstanding, the following could be concluded. (i) The primate model is ideal for investigating Candida-associated denture stomatitis since both erythematous and pseudomembranous lesions have been produced in monkeys with prosthetic plates; they are, however, expensive and difficult to obtain and maintain. (ii) The rat model (both Sprague-Dawley and Wistar) is well proven for observing chronic oral candidal colonization and infection, due to the ease of breeding and handling and their ready availability. (iii) Mice are similar, but in addition there are well characterized variants simulating immunologic and genetic abnormalities (e.g., athymic, euthymic, murine-acquired immune deficiency syndrome, and severe combined immunodeficient models) and hence are used for short-term studies relating the host immune response and oral candidiasis. Nonetheless, an ideal, relatively inexpensive model representative of the human oral environment in ecological and microbiological terms is yet to be described. Until such a model is developed, researchers should pay attention to standardization of the experimental protocols described here to obtain broadly comparable and meaningful data.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date (Print): 2014
                Publication date (Electronic): 18 February 2014
                Volume: 2014
                Electronic Location Identifier: 509325
                Affiliations
                1Department of Pathology, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata, Osaka 573-0101, Japan
                2Laboratory of Clinicopathological Therapeutics, Faculty of Pharmaceutical Sciences, Hiroshima International University, Kure, Hiroshima 737-0112, Japan
                Author notes

                Academic Editor: Norman Cameron

                Article
                DOI: 10.1155/2014/509325
                PMC ID: 3945120
                SO-VID: ad2c14ef-61f4-4853-9f1c-acac08dffae6
                Copyright © Copyright © 2014 Tomoya Sano et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 18 November 2013
                Date revision received : 7 January 2014
                Date accepted : 7 January 2014
                Categories
                Subject: Research Article

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