Abstract
Inflammation is a complex systemic response evolved to cope with cellular injury, either due to infectious agents or, in general, with sporadic events challenging tissue integrity and function. Researchers involved in different fields have the tendency to look at the inflammatory response with different angles, according to their specific interest. Established its complexity, one of the most evident features of the inflammatory response is the generation of a pro-oxidative environment due to the production of high fluxes of pro-oxidant species. This production begins locally, close to the sites of tissue damage or infection, but eventually becomes a chronic challenge for the organism, if the inflammatory response is not properly controlled. In this review, we focus on this specific aspect of chronic, low-level sub-clinical inflammatory response. We propose the term “OxInflammation” as a novel operative term describing a permanent pro-oxidative feature that interact, in a positive feed-back manner, to a not yet clinically detectable inflammatory process, leading in a long run (chronically) to a systemic/local damage, as a consequence of the cross talk between inflammatory, and oxidative stress mediators. Therefore, it could be useful to analyze inflammatory markers in pathologies where there is an alteration of the redox homeostasis, although an inflammatory status is not clinically evident.
Highlights
Reviewed by: Houzao Chen, Institute of Basic Medical Sciences (CAMS), China Wenbo Zhang, University of Texas Medical Branch, United States
There are other cellular constituents that directly participate in redox processes; for example, peroxisomes are rich in CAT, allowing them to cope with the elevated propensity of these organelles for the generation of superoxide anion and hydrogen peroxide (Davies et al, 2017)
Other widely used marker of oxidative stress are the byproducts generated by oxidative modification of proteins, such as carbonyl-groups 3-nitrotyrosine, advanced oxidation protein products (AOPP), and those derived by modification of DNA, 8-oxo-7, 8-dihydro-2′-deoxyguanosine (8-OHdG), and RNA, 8-hydroxyguanosine (8-OHG), and carbohydrates (DalleDonne et al, 2006; Frijhoff et al, 2015)
Summary
Inflammation is a tissue response to damage characterized by a fine regulated set of events in which several cell type are sequentially activated and able to secrete key mediators (Calder et al, 2013). The main cells involved in the inflammatory responses are neutrophils, macrophages, and other immune cells, controlled by chemical mediators generically called cytokines and chemokines (Mantovani et al, 2011). The first step of an inflammatory response is the up-regulation of genes encoding for cytokines, chemokines, and other mediators, through activation of transcription factors such as nuclear factor κ B (NF-κB), activator protein-1 (AP-1), nuclear factor of activated T cells (NFAT), and signal transducer and activator of transcription-3 (STAT3) (Smale, 2010)
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