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Free Radicals and Pathogens – Role for Reactive Intermediates in Innate Immunity

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Systems Biology of Free Radicals and Antioxidants

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Abstract

Microorganisms that enter the body and cause disease are referred to as pathogenic microorganisms or pathogens. Microbial invasion is detected by pattern recognition receptors, and innate defense mechanisms including production of reactive oxygen and nitrogen species (ROS and RNS) and pro-inflammatory signaling are subsequently triggered within minutes of bacterial attack. Thereby, innate immunity is regarded to be the first line of host defense and acts through general antimicrobial mechanisms such as acidification, the production of antimicrobial peptides or enzymes, and the generation of toxic molecules including ROS/RNS. ROS-producing enzymes are located in the cytoplasmic and phagosome membranes and to a minor degree in the cytosol, in mitochondria, in the endoplasmic reticulum, and in peroxisomes in all aerobic cells. In order to prevent potentially damaging effects of ROS production, cells produce several endogenous enzymes such as superoxide dismutase (SOD), catalase, or glutathione peroxidase, which reduce superoxide to hydrogen peroxide and hydrogen peroxide to water. This chapter mainly focuses on ROS and RNS production in cells of the innate immune system with regard to antimicrobial activity and the microbial strategies of pathogens to escape from host oxidative defense mechanisms.

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Authors and Affiliations

  1. Institute for Experimental Medicine, Christian-Albrechts-University Kiel and Research Center Borstel, Parkallee 29, 23845, Borstel, Germany

    Natalie Steck & Guntram A. Grassl

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  1. Natalie Steck
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Correspondence to Guntram A. Grassl .

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  1. Department of Pharmacology and Therapeutics, University of British Colombia, Vancouver, British Columbia, Canada

    Ismail Laher

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Steck, N., Grassl, G.A. (2014). Free Radicals and Pathogens – Role for Reactive Intermediates in Innate Immunity. In: Laher, I. (eds) Systems Biology of Free Radicals and Antioxidants. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-30018-9_103

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