Abstract
Oxidative stress is key in immune defense against fungal infections, such as those caused by Sporothrix schenckii, the dimorphic fungus responsible for sporotrichosis. Phagocytic cells utilize oxidative stress as a crucial mechanism to control pathogen spread. During S. schenckii infection, phagocytic cells recognize pathogen-associated molecular patterns (PAMPs) on their surface through conserved transmembrane or soluble receptors, known as pattern recognition receptors (PRRs). This recognition triggers a cascade of immune responses, including the generation reactive oxygen species (ROS) essential for pathogen elimination. However, S. schenckii has developed sophisticated mechanisms to evade and counteract this response, contributing to its persistence in the host. These mechanisms include the production of antioxidant enzymes, alterations to its cell wall (CW), and the production of melanin, which helps neutralize oxidative stress. In addition, S. schenckii modulates the production of other proteins, such as moonlighting proteins, suggested to have roles in immune evasion and stress response, helping its survival in the host. These strategies, along with the modulation of gene expression, allow the fungus to survive and persist inside the immune system's hostile environment, facilitating the progression of the infection. Understanding these interactions between phagocytic cells and S. schenckii is key to developing more effective therapeutic strategies to combat sporotrichosis.