Candida albicans is an opportunistic fungal pathogen. The ability of Candida to adhere to host cells is key to this pathogenesis and cell surface hydrophobicity (CSH) is key to adhesion. The cell wall of Candida contains hydrophobic proteins which are believed to be involved in adhesion. Previous studies in the laboratory suggested that surface protein glycosylation influences exposure of the hydrophobic proteins. This suggestion is supported by freeze fracture electron micrographs of hydrophilic and hydrophobic cells, studies showing the effect of CSH on Candida adhesion to various surfaces and studies demonstrating the involvement of surface glycoproteins in adhesion to the same types of surfaces. This proposal addresses several remaining questions related to this hypothesis: A. What is the composition of the hydrophilic cell wall, and how does it compare to that of hydrophobic cell walls? B. How does treatment with antifungal agents affect cell wall hydrophobicity? C. Are these changes reflected in changes in cell wall composition? D. Which proteins are involved in cell surface changes? Although these are somewhat disparate questions, they share a common goal. The results from each feed into and refine the others. All are directed towards a clearer picture of how the Candida cell wall interacts with its environment, providing valuable insights into the mechanism and regulation of Candida adhesion.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32AI009428-01
Application #
2059525
Study Section
Immunology, Virology, and Pathology Study Section (IVP)
Project Start
1996-01-31
Project End
Budget Start
1995-09-01
Budget End
1996-08-31
Support Year
1
Fiscal Year
1995
Total Cost
Indirect Cost
Name
University of Virginia
Department
Pathology
Type
Schools of Medicine
DUNS #
001910777
City
Charlottesville
State
VA
Country
United States
Zip Code
22904