Journal
BIOMOLECULES
Volume 5, Issue 1, Pages 142-165Publisher
MDPI
DOI: 10.3390/biom5010142
Keywords
fungal pathogenesis; Candida albicans; oxidative stress; stress signaling
Categories
Funding
- BBSRC [BB/K016393/1]
- MRC-DTP studentship
- NIHR Newcastle Biomedical Research Centre
- Wellcome Trust Strategic Award for Medical Mycology and Fungal Immunology [097377/Z/11/Z]
- BBSRC [BB/K016393/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/K016393/1] Funding Source: researchfish
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Candida albicans is a major fungal pathogen of humans, causing approximately 400,000 life-threatening systemic infections world-wide each year in severely immunocompromised patients. An important fungicidal mechanism employed by innate immune cells involves the generation of toxic reactive oxygen species (ROS), such as superoxide and hydrogen peroxide. Consequently, there is much interest in the strategies employed by C. albicans to evade the oxidative killing by macrophages and neutrophils. Our understanding of how C. albicans senses and responds to ROS has significantly increased in recent years. Key findings include the observations that hydrogen peroxide triggers the filamentation of this polymorphic fungus and that a superoxide dismutase enzyme with a novel mode of action is expressed at the cell surface of C. albicans. Furthermore, recent studies have indicated that combinations of the chemical stresses generated by phagocytes can actively prevent C. albicans oxidative stress responses through a mechanism termed the stress pathway interference. In this review, we present an up-date of our current understanding of the role and regulation of oxidative stress responses in this important human fungal pathogen.
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