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Candida glabrata and Candida albicans; dissimilar tissue tropism and infectivity in a gnotobiotic model of mucosal candidiasis

  1. Caroline Westwater1,
  2. David A. Schofield2,
  3. Peter J. Nicholas3,
  4. Emily E. Paulling3,
  5. Edward Balish3

Article first published online: 11 JUL 2007

DOI: 10.1111/j.1574-695X.2007.00287.x

Issue

FEMS Immunology & Medical Microbiology

FEMS Immunology & Medical Microbiology

Volume 51, Issue 1, pages 134–139, October 2007

Additional Information

How to Cite

Westwater, C., Schofield, D. A., Nicholas, P. J., Paulling, E. E. and Balish, E. (2007), Candida glabrata and Candida albicans; dissimilar tissue tropism and infectivity in a gnotobiotic model of mucosal candidiasis. FEMS Immunology & Medical Microbiology, 51: 134–139. doi: 10.1111/j.1574-695X.2007.00287.x

Author Information

  1. 1

    Department of Stomatology, Medical University of South Carolina, Charleston, SC, USA

  2. 2

    Guild Associates Inc., Charleston, SC, USA

  3. 3

    Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA

*Correspondence: Edward Balish, Medical University of South Carolina, Department of Microbiology and Immunology, BSB-201, P.O. Box 250504, 173 Ashley Avenue, Charleston, SC 29425, USA. Tel.: +1 843 792 6317; fax: +1 843 792 2464; e-mail: balish@musc.edu

Publication History

  1. Issue published online: 20 JUL 2007
  2. Article first published online: 11 JUL 2007
  3. Received 2 March 2007; revised 8 May 2007; accepted 19 May 2007.First published online 11 July 2007.

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Keywords:

  • candidiasis;
  • animal models;
  • immunodeficient;
  • Candida albicans;
  • Candida glabrata;
  • mucosal infection

Abstract

Germ-free transgenic epsilon 26 (Tgɛ26) mice, deficient in both natural killer (NK)- and T-cells, were inoculated (orally) with each of two Candida glabrata (BG2 or BG1003) or Candida albicans (CAF2-1 or SC5314) strains. Candida glabrata- or C. albicans-colonized mice exhibited similar numbers of viable Candida in the alimentary tract. Neither C. glabrata nor C. albicans caused systemic candidiasis of endogenous (alimentary tract) origin. Candida albicans invaded oroesophageal (tongue, palate, esophagus) and keratinized gastric tissues, evoked hyperkeratosis and a prominent, chronic, granulocyte-dominated, inflammatory response in all infected tissues, stimulated the production of splenic granulocytes and was lethal for the mice within 3–5 weeks after oral colonization. The two C. glabrata strains colonized the alimentary tract and penetrated into the keratinized (cardia-antrum) gastric tissues, but in contrast to C. albicans, were unable to infect oroesophageal tissues. Furthermore, C. glabrata strains were not lethal for the Tgɛ26 mice, and did not evoke an inflammatory response in colonized gastric tissues or stimulate the production of splenic granulocytes. This ‘stealth-like’ behavior could explain the ability of C. glabrata to persist in infected tissues and survive as a commensal in the alimentary tract.

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