Oxidative stress in Candida albicans infection

Abstract

Candidiasis, one of the most common hospital-acquired infections of humans, is predominantly caused by the fungi Candida albicans. In most healthy individuals, C. albicans can be found as part of the normal microbial flora in the skin, oral cavity, digestive tract, and female reproductive tract without causing any infection. However, in the case of immunocompromised patients or in situations where normal microbiota is disrupted, the fungi can cause mild to severe infection. After entering the host system, C. albicans cells are exposed to a wide variety of toxic chemicals, most important of which being the reactive oxygen species (ROS) produced by host phagocytes, such as neutrophils and macrophages. The pathogenic fungi, on its part, elicit a strong response against the ROS by activating/regulating multiple signaling pathways involving the stress-activated protein kinase Hog1, the DNA damage kinase Rad53, and the transcription factor Cap1 in order to survive under the oxidative stress condition. In this chapter, we have tried to depict a brief overview of this host-C. albicans interaction while focusing more on the oxidative stress generated by the host phagocytes and the response of the C. albicans cells against this deadly attack.