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Oxidative Stress, Pathophysiology, and Immunity in Brucellosis

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Oxidative Stress in Microbial Diseases

Abstract

The Brucella being obligate intracellular parasite, its survival in host requires the ability to overcome host immune system as well as host oxidative stress mechanism. In general, Brucellosis induces rise in host oxidative stress with weakening of the host’s antioxidant defense system. The survival of Brucella to host oxidative and antioxidant system depends on the presence of superoxide dismutase (SOD) and catalase in Brucella. Of these, SOD acts as a major antioxidant enzyme in Brucella pathophysiology. Brucella possesses two SODs, SodA and SodC, that directly detoxify superoxide radicals. SodA resides in the cytoplasmic compartment, while SodC in the periplasm of Brucella strains and exclusively detoxifies superoxide radical within the cellular compartments in which bacteria reside. The endogenously produced superoxide radicals of respiratory metabolism are detoxified by SodA, while exogenously generated during respiratory burst in host phagocytes are typically detoxified by SodC. The catalase neutralizes H2O2 produced during the process. The catalase is mainly constrained to the periplasm and provides protection against H2O2 produced during the immune response provoked against Brucella infection. Regulation of this enzyme along with detoxification of superoxide radicals with SOD is mainly responsible for the adaptation process of Brucella and allows its survival under hostile conditions.

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Kumar, A., Rahal, A., Gupta, V.K. (2019). Oxidative Stress, Pathophysiology, and Immunity in Brucellosis. In: Chakraborti, S., Chakraborti, T., Chattopadhyay, D., Shaha, C. (eds) Oxidative Stress in Microbial Diseases. Springer, Singapore. https://doi.org/10.1007/978-981-13-8763-0_20

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