Mechanisms controlling bacterial infection in myeloid cells under hypoxic conditions
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Cellular and Molecular Life Sciences
REVIEW
Mechanisms controlling bacterial infection in myeloid cells under hypoxic conditions Inaya Hayek1 · Valentin Schatz2 · Christian Bogdan1,3 · Jonathan Jantsch2 · Anja Lührmann1,3 Received: 8 February 2020 / Revised: 8 September 2020 / Accepted: 9 October 2020 © The Author(s) 2020
Abstract Various factors of the tissue microenvironment such as the oxygen concentration influence the host–pathogen interaction. During the past decade, hypoxia-driven signaling via hypoxia-inducible factors (HIF) has emerged as an important factor that affects both the pathogen and the host. In this chapter, we will review the current knowledge of this complex interplay, with a particular emphasis given to the impact of hypoxia and HIF on the inflammatory and antimicrobial activity of myeloid cells, the bacterial responses to hypoxia and the containment of bacterial infections under oxygen-limited conditions. We will also summarize how low oxygen concentrations influence the metabolism of neutrophils, macrophages and dendritic cells. Finally, we will discuss the consequences of hypoxia and HIFα activation for the invading pathogen, with a focus on Pseudomonas aeruginosa, Mycobacterium tuberculosis, Coxiella burnetii, Salmonella enterica and Staphylococcus aureus. This includes a description of the mechanisms and microbial factors, which the pathogens use to sense and react to hypoxic conditions. Keywords Hypoxia · HIF1α · Infection · Bacteria · Metabolism · Macrophages · Neutrophils · Dendritic cells Abbreviations ATP Adenosine triphosphate DCs Dendritic cells DSS Dextran sulfate sodium DMOG Dimethyloxalylglycine (Dos)R Dormancy survival regulator HIF Hypoxia-inducible factors IDO Indoleamine 2,3-dioxygenase iNOS or NOS2 Inducible or type 2 nitric oxide synthase IFNγ Interferon γ IL Interleukin LDH-A Lactate dehydrogenase-A LPS Lipopolysaccharide * Jonathan Jantsch [email protected] * Anja Lührmann anja.luehrmann@uk‑erlangen.de 1
Mikrobiologisches Institut, Klinische Mikrobiologie, Immunologie und Hygiene, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, 91054 Erlangen, Germany
2
Institut für Klinische Mikrobiologie und Hygiene, Universitätsklinikum Regensburg, Universität Regensburg, 93053 Regensburg, Germany
3
Medical Immunology Campus Erlangen, FAU Erlangen-Nürnberg, 91054 Erlangen, Germany
MtrAB M. tuberculosis Two-component regulatory system MtrA/MtrB NET Neutrophil extracellular traps NO Nitric oxide OXPHOS Oxidative phosphorylation PHOX Phagocyte NADPH-oxidase PMN Polymorphonuclear neutrophils PHDs Prolyl hydroxylases PKM2 Pyruvate kinase M2 RNS Reactive nitrogen species ROS Reactive oxygen species SPI-2 Salmonella Pathogenicity island 2 TCA Tricarboxylic acid cycle VEGF Vascular endothelial growth factor
Introduction Myeloid cells are the first line of defense against bacterial infections. They are equipped with an arsenal of mechanisms to prevent spreading of the intruders, to alert the adaptiv
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