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Zinc accelerates respiratory burst termination in human PMN.

Authors
  • Droste, Annika1
  • Chaves, Gustavo2
  • Stein, Stefan3
  • Trzmiel, Annette3
  • Schweizer, Matthias4
  • Karl, Hubert5
  • Musset, Boris6
  • 1 Center of Physiology, Pathophysiology and Biophysics, Paracelsus Medical University, Nuremberg, Germany; Department of Gynecology and Obstetrics, Johannes Gutenberg University, Mainz, Germany. , (Germany)
  • 2 Center of Physiology, Pathophysiology and Biophysics, Paracelsus Medical University, Nuremberg, Germany. , (Germany)
  • 3 Flow Cytometry Unit, Institute for Tumor Biology and Experimental Therapy, Georg-Speyer-Haus, Frankfurt, Germany. , (Germany)
  • 4 Federal Institute for Vaccines and Biomedicines, Paul-Ehrlich-Institut, Langen, Germany. , (Germany)
  • 5 Department efi, Technische Hochschule Nürnberg Georg Simon Ohm, Nuremberg, Germany. , (Germany)
  • 6 Center of Physiology, Pathophysiology and Biophysics, Paracelsus Medical University, Nuremberg, Germany; Center of Physiology, Pathophysiology and Biophysics, Paracelsus Medical University, Salzburg, Austria. Electronic address: [email protected] , (Austria)
Type
Published Article
Journal
Redox Biology
Publisher
Elsevier
Publication Date
Sep 17, 2021
Volume
47
Pages
102133–102133
Identifiers
DOI: 10.1016/j.redox.2021.102133
PMID: 34562872
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The respiratory burst of phagocytes is essential for human survival. Innate immune defence against pathogens relies strongly on reactive oxygen species (ROS) production by the NADPH oxidase (NOX2). ROS kill pathogens while the translocation of electrons across the plasma membrane via NOX2 depolarizes the cell. Simultaneously, protons are released into the cytosol. Here, we compare freshly isolated human polymorphonuclear leukocytes (PMN) to the granulocytes-like cell line PLB 985. We are recording ROS production while inhibiting the charge compensating and pH regulating voltage-gated proton channel (HV1). The data suggests that human PMN and the PLB 985 generate ROS via a general mechanism, consistent of NOX2 and HV1. Additionally, we advanced a mathematical model based on the biophysical properties of NOX2 and HV1. Our results strongly suggest the essential interconnection of HV1 and NOX2 during the respiratory burst of phagocytes. Zinc chelation during the time course of the experiments postulates that zinc leads to an irreversible termination of the respiratory burst over time. Flow cytometry shows cell death triggered by high zinc concentrations and PMA. Our data might help to elucidate the complex interaction of proteins during the respiratory burst and contribute to decipher its termination. Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.

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