Morpholino Drug Development
Candida albicans Growth Forms – pseudohaphae, clamydospores and hyphae
Guild BioSciences is performing drug discovery using anti-sense morpholino technology. The focus of the research is evaluating the efficacy of morpholino oligomers in combating oral candidiasis.
Candida albicans is a fungal pathogen of considerable significance in humans. It has been estimated that up to 80% of the human population are asymptomatic carriers of Candida species, typically in the oral cavity, gastrointestinal tract, and female genital tract. Given such a high level of exposure, Candida has become the leading cause of fungal infection in humans. Although it is a common commensal of the oral cavity and gastrointestinal tract, under physiological or immunological changes to the host, this opportunistic pathogen can cause disease. For example, C. albicans is responsible for a variety of infections, ranging from mucosal infections to life-threatening systemic disease. In fact, C. albicans is a serious cause of morbidity and mortality, and even with anti-fungal treatment, patients with invasive (or systemic) candidiasis have an extremely poor prognosis. Moreover, with a growing population of elderly, diabetic, and immunosuppressed (e.g., cancer or HIV) patients, the incidence of candidiasis is predicted to increase.
Guild BioSciences is always interested in extending this research through collaboration, exploring new or non-traditional opportunities, and developing marketable products. Please contact us to explore ways in which we can work together.
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Listed below are the abstracts and links to oral candidiasis and corresponding drug discovery research publications and conference presentations made by Guild BioSciences scientists.
Schofield, D.A., Frank, M.B., Balish, E. and Westwater, C. 2008. In vivo transcriptional profiling of Candida albicans during the commensal to pathogenic transition. American Society of Microbiology meeting on Candida and Candidiasis, Jersey, NJ.
Westwater, C., Balish E., Warner, T.F., Nicholas, P.J., Paulling, E.E. and Schofield, D.A. 2007. Susceptibility of gnotobiotic transgenic mice (Tge26) with combined deficiencies in natural killer cells and T cells to wild-type and hyphal signaling-defective mutants of Candida albicans. Journal of Medical Microbiology, 56(9):1138-1144.
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 and Medical Microbiology, 51(1):134-139.
Schofield, D.A., Westwater, C., Warner, T., and Balish, E. 2005. Differential Candida albicans lipase gene expression during alimentary tract colonization and infection. FEMS Microbiology Letters, 244:359-365.
Westwater, C., Balish, E. and Schofield, D.A. 2005. Candida albicans-conditioned media protects cells from oxidative stress: a possible link between quorum-sensing and oxidative stress resistance. Eukaryotic Cell, 4(10):1654-1661.
Schofield, D.A., Westwater, C. and Balish, E. 2004. ß-defensin expression in immunocompetent and immunodeficient germfree and Candida albicans monoassociated mice. Journal of Infectious Diseases, 190:1327-1334.
Schofield, D.A., Westwater, C., Paulling, E.E., Nicholas, P.J. and Balish, E. 2003. Detection of Candida albicans mRNA from formalin-fixed, paraffin-embedded mouse tissue by nested reverse transcription-PCR. Journal of Clinical Microbiology, 41:831-834.
