@article{mbs:/content/journal/jmm/10.1099/jmm.0.47110-0, author = "Westwater, Caroline and Balish, Edward and Warner, Thomas F. and Nicholas, Peter J. and Paulling, Emily E. and Schofield, David A.", title = "Susceptibility of gnotobiotic transgenic mice (Tgϵ26) with combined deficiencies in natural killer cells and T cells to wild-type and hyphal signalling-defective mutants of Candida albicans", journal= "Journal of Medical Microbiology", year = "2007", volume = "56", number = "9", pages = "1138-1144", doi = "https://doi.org/10.1099/jmm.0.47110-0", url = "https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.47110-0", publisher = "Microbiology Society", issn = "1473-5644", type = "Journal Article", keywords = "NK, natural killer", keywords = "IL, interleukin", keywords = "GF, germfree", keywords = "RNI, reactive nitrogen intermediates", keywords = "ROI, reactive oxygen intermediates", keywords = "MIP, macrophage inflammatory protein", keywords = "TNFα, tumour necrosis factor alpha", abstract = "Germfree transgenic epsilon 26 mice (Tgϵ26), 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 Tgϵ26 mice, whereas the mice colonized with the mutant strains survived. Death of the Tgϵ26-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.", }