Oxidative Stress in Host–Pathogen Interactions: Molecular Mechanisms, Biomarkers, and Therapeutic Strategies

Oxidative stress is now thought to be one of the major factors regulating the course of host-pathogen interactions and the evolution of infectious illnesses. When infected, the immune cells generate reactive oxygen species (ROS) and reactive nitrogen species (RNS) as part of the body’s defense against invading microbes. These compounds are important in the control of microbial growth, but their overproduction may cause disturbances of redox equilibrium and oxidative damage to lipids, proteins and DNA. Simultaneously, many infections have evolved complex defense strategies to survive oxidative stress, increase their virulence and thwart antimicrobial therapy. This review summarizes current knowledge on oxidative stress in bacterial, viral, fungal and parasitic infections with a focus on biochemical pathways of ROS and RNS generation, main sources of oxidative stress during infection and microbial adaptive strategies to counteract oxidative damage. It talks about the clinical value of oxidative stress biomarkers such as malondialdehyde (MDA), total oxidant status (TOS), total antioxidant capacity (TAC), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), 8-hydroxy-2′-deoxyguanosine (8-OHdG) and protein carbonyls in assessing disease severity and therapeutic response. Emerging therapeutic techniques are also discussed, including antioxidant therapy, nanotechnology-based approaches, suppression of microbial antioxidant defense mechanisms, and biomarker-guided personalized medicine. A greater knowledge of redox regulation in infection may help in the development of novel diagnostic tools and tailored therapeutics to improve infection management, while maintaining the balance between efficient antimicrobial immunity and protection of host tissue.