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Virulence mechanisms of coccidioides
Chiung-Yu Hung1, Jianmin Xue, Garry T Cole
1Department of Biology, University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249-0662, USA. chiungyu.hung@utsa.edu
Annals of the New York Academy of Sciences
|May 22, 2007
Summary
Coccidioides fungus evades immune defenses through a glycoprotein shield and by depleting immune cells of essential nutrients. This fungal pathogen also triggers host enzymes, leading to tissue damage and increased infection severity.
Area of Science:
- Mycology
- Immunology
- Pathogenesis
Background:
- Coccidioides is a fungal respiratory pathogen causing disease in immunocompromised and immunocompetent individuals.
- Understanding Coccidioides survival mechanisms is crucial for developing effective treatments.
Purpose of the Study:
- To elucidate the mechanisms by which Coccidioides survives within the host.
- To investigate the roles of spherule outer wall glycoprotein (SOWgp), arginase I, and urease in Coccidioides pathogenesis.
Main Methods:
- Analysis of SOWgp production and presentation on Coccidioides endospores.
- Assessment of host arginase I and Coccidioides urease activity during infection.
- Measurement of nitric oxide (NO), L-arginine, ornithine, urea, and ammonia concentrations at infection sites.
Main Results:
- SOWgp production modulates host immune response, compromising cell-mediated immunity.
- Depletion of SOWgp on endospores hinders host recognition during vulnerable stages.
- Elevated host arginase I and fungal urease contribute to tissue damage and immune suppression via L-arginine metabolism and ammonia production.
Conclusions:
- Coccidioides employs multiple strategies, including immune evasion via SOWgp and host-derived enzyme manipulation, to ensure survival and proliferation.
- Ammonia and urease contribute to increased infection severity by impairing host immunity and causing tissue damage.
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