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J Med Microbiol 56 (2007), 1138-1144; DOI: 10.1099/jmm.0.47110-0
© 2007 Society for General Microbiology
ISSN 1473-5644

Susceptibility of gnotobiotic transgenic mice (Tg{epsilon}26) with combined deficiencies in natural killer cells and T cells to wild-type and hyphal signalling-defective mutants of Candida albicans

Caroline Westwater1, Edward Balish2, Thomas F. Warner3, Peter J. Nicholas2, Emily E. Paulling2 and David A. Schofield2,{dagger}

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

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

3 Department of Surgical Pathology, University of Wisconsin Medical School, Madison, WI, USA

Correspondence
David A. Schofield
dschofield{at}guildassociates.com

Received 5 December 2006
Accepted 18 April 2007

Germfree transgenic epsilon 26 mice (Tg{epsilon}26), deficient in natural killer cells and T cells, were colonized (alimentary tract) with Candida albicans wild-type or each of two hyphal transcription factor signalling mutant strains (efg1/efg1, efg1/efg1 cph1/cph1). Each Candida strain colonized the alimentary tract, infected keratinized gastric tissues to a similar extent, and induced a granulocyte-dominated inflammatory response in infected tissues. Both wild-type and mutant strains formed hyphae in vivo and were able to elicit an increase in cytokine [tumour necrosis factor alpha, interleukin (IL)-10 and IL-12] and chemokine (KC and macrophage inflammatory protein-2] mRNAs in infected tissues; however, administration of the wild-type strain was lethal for the Tg{epsilon}26 mice, whereas the mice colonized with the mutant strains survived. Death of the Tg{epsilon}26-colonized mice appeared to be due to occlusive oesophageal candidiasis, and not to disseminated candidiasis of endogenous origin. In contrast, the mutant strains exhibited a significantly reduced capacity to infect (frequency and severity) oro-oesophageal (tongue and oesophagus) tissues. Therefore, the two hyphal signalling-defective mutants were less able to infect oro-oesophageal tissues and were non-lethal, but retained their ability to colonize the alimentary tract with yeast and hyphae, infect keratinized gastric tissues, and evoke an inflammatory response in orogastric tissues.

Abbreviations: GF, germfree; IL, interleukin; MIP, macrophage inflammatory protein; NK, natural killer; RNI, reactive nitrogen intermediates; ROI, reactive oxygen intermediates; TNF{alpha}, tumour necrosis factor alpha.

{dagger}Present address: Guild Associates Inc., 1313B Ashley River Road, Charleston, SC 29407, USA.




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E. Balish
A URA3 null mutant of Candida albicans (CAI-4) causes oro-oesophageal and gastric candidiasis and is lethal for gnotobiotic, transgenic mice (Tg{epsilon}26) that are deficient in both natural killer and T cells
J. Med. Microbiol., March 1, 2009; 58(3): 290 - 295.
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