targeting nuclear factor erythroid 2-related factor transcription factor/hemoxygenase 1 (nrf2//ho-1) antioxidant signaling pathway in brucella infection

Human health is at serious risk from brucellosis, a zoonotic infection brought on by the genus brucella, especially in areas where livestock is common. the clinical manifestations of brucellosis in humans are diverse, often beginning with nonspecific flu-like symptoms such as fever, chills, malaise, and arthralgia. the immune response to brucella infection is complex, involving various cytokines and immune mediators, which can be influenced by the host’’s genetic background and environmental factors. preventive measures primarily focus on livestock vaccination and public health education regarding the risks associated with unpasteurized dairy products and direct animal contact. the pathophysiology of brucella is significantly influenced by oxidative stress, primarily in its interactions with the host immune system. it is known that brucella species cause oxidative stress in their host cells, which activates a number of different biological processes, including the nuclear factor erythroid 2-related factor transcription factor (nrf2) pathway. nrf2 is a transcription factor that governs the expression of antioxidant proteins, which safeguard against oxidative damage caused by injury and inflammation. activation of nrf2 has been shown to upregulate ho-1, which is involved in modulating the immune response. the enzyme’’s activity regulates proinflammatory cytokines and anti-inflammatory environment, aiding brucella in evading the host’’s immune defenses. therefore, therapeutic strategies that enhance nrf2 activation could improve the host’’s immune response while limiting the survival advantage of brucella. future research should continue to explore the therapeutic potential of targeting the nrf2/ho-1 axis in various infectious diseases, particularly brucella infection, to improve clinical outcomes.