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      Oxycytosis and the role of triboelectricity and oxidation in bacteria clearing from the bloodstream

      review-article
      *
      European Journal of Microbiology & Immunology
      Akadémiai Kiadó
      innate immunity, phagocytosis, oxycytosis, bacteremia, sepsis

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          Abstract

          Until recently, little was known about the mechanism for killing and clearing bacteria from the bloodstream. Leukocyte phagocytosis could not be a mechanism for catching, killing and removing bacteria from the bloodstream because of many reasons. Recently accumulated data have led to the conclusion that in bacteremia, bacteria are quickly removed from the blood and erythrocytes are the main cells that capture, kill and remove bacteria. Data were also obtained that erythrocytes catch bacteria by triboelectric charge attraction and kill them by oxygen released from oxyhemoglobin. This phenomenon has been named oxycytosis by analogy with the term phagocytosis. Oxycytosis has been discussed in a number of published articles, but the specific mechanism of triboelectric charging and the mechanism of killing bacteria by oxidation, have not yet been detailed. The purpose of this review is to provide a more detailed explanation of the process of triboelectric charging and capture of bacteria by erythrocytes and destruction of bacteria by oxidation. For the first time, the review presents various variants of oxycytosis (two-stage, three-stage, multi-stage), depending on the resistance of the pathogen to oxidation. The review also discusses the biological significance of oxycytosis and its impact on the understanding of bacteremia and sepsis.

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          Most cited references59

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          Red cell membrane: past, present, and future.

          As a result of natural selection driven by severe forms of malaria, 1 in 6 humans in the world, more than 1 billion people, are affected by red cell abnormalities, making them the most common of the inherited disorders. The non-nucleated red cell is unique among human cell type in that the plasma membrane, its only structural component, accounts for all of its diverse antigenic, transport, and mechanical characteristics. Our current concept of the red cell membrane envisions it as a composite structure in which a membrane envelope composed of cholesterol and phospholipids is secured to an elastic network of skeletal proteins via transmembrane proteins. Structural and functional characterization of the many constituents of the red cell membrane, in conjunction with biophysical and physiologic studies, has led to detailed description of the way in which the remarkable mechanical properties and other important characteristics of the red cells arise, and of the manner in which they fail in disease states. Current studies in this very active and exciting field are continuing to produce new and unexpected revelations on the function of the red cell membrane and thus of the cell in health and disease, and shed new light on membrane function in other diverse cell types.
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            How bacterial pathogens colonize their hosts and invade deeper tissues.

            Bacterial pathogens have evolved a wide range of strategies to colonize and invade human organs, despite the presence of multiple host defense mechanisms. In this review, we will describe how pathogenic bacteria can adhere and multiply at the surface of host cells, how some bacteria can enter and proliferate inside these cells, and finally how pathogens may cross epithelial or endothelial host barriers and get access to internal tissues, leading to severe diseases in humans.
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              DNA damage and oxygen radical toxicity.

              A major portion of the toxicity of hydrogen peroxide in Escherichia coli is attributed to DNA damage mediated by a Fenton reaction that generates active forms of hydroxyl radicals from hydrogen peroxide, DNA-bound iron, and a constant source of reducing equivalents. Kinetic peculiarities of DNA damage production by hydrogen peroxide in vivo can be reproduced by including DNA in an in vitro Fenton reaction system in which iron catalyzes the univalent reduction of hydrogen peroxide by the reduced form of nicotinamide adenine dinucleotide (NADH). To minimize the toxicity of oxygen radicals, the cell utilizes scavengers of these radicals and DNA repair enzymes. On the basis of observations with the model system, it is proposed that the cell may also decrease such toxicity by diminishing available NAD(P)H and by utilizing oxygen itself to scavenge active free radicals into superoxide, which is then destroyed by superoxide dismutase.
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                Author and article information

                Journal
                Eur J Microbiol Immunol (Bp)
                Eur J Microbiol Immunol (Bp)
                EUJMI
                European Journal of Microbiology & Immunology
                Akadémiai Kiadó (Budapest )
                2062-509X
                2062-8633
                20 May 2021
                10 July 2021
                : 11
                : 2
                : 23-28
                Affiliations
                Mamikonyanz 38-38, Yerevan, 0014, Armenia
                Author notes
                *Corresponding author. Tel.: +374 77255295. E-mail: haykminasyan@ 123456rambler.ru
                Article
                10.1556/1886.2021.00008
                8287977
                34019486
                7e9f2a25-38bf-48f5-8962-a4b2dae95935
                © 2021, The Author(s)

                Open Access. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes - if any – are indicated.

                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 61, Pages: 6
                Categories
                Review Paper

                innate immunity,phagocytosis,oxycytosis,bacteremia,sepsis
                innate immunity, phagocytosis, oxycytosis, bacteremia, sepsis

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