The Role of Reactive Oxygen Species in Innate Immunity

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (15 March 2023) | Viewed by 2574

Special Issue Editors

Institute for Medical Microbiology, Immunology and Hygiene, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50935 Cologne, Germany
Interests: macrophages, reactive oxygen species, mitochondria, redox signaling, infection

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Guest Editor
Department of Biology & Nutrafood Center, University of Pisa, 56126 Pisa, Italy
Interests: ectonucleotidases; protective genes; redox biology; apolipoprotein A-I; cancer drug resistance

Special Issue Information

Dear Colleagues,

The importance of ROS for innate immunity has been demonstrated by many studies and their functions comprise direct and indirect antimicrobial activity. The most prominent direct antimicrobial function is the ROS-mediated inactivation and elimination of foreign organisms like bacteria, viruses and parasites. Indirect functions of ROS include the broad range of redox-regulated immune processes, such as modulation of pro- and anti-inflammatory signaling pathways, induction of inflammasomes and chemotaxis. The spectrum of ROS-related functions in innate immunity is as complex as the various innate immune cell types and their interplay. Phagocytes, including macrophages or neutrophils are the mainly investigated immune cell types concerning ROS-related processes, but also in other leukocytes, such as mast cells or natural killer cells, ROS play important roles for innate immune defense.

In this Special Issue, we want to invite researchers to contribute both original research and review articles. Studies that provide strong mechanistic insights regarding the precise roles of ROS in innate immune cells are still scarce. Therefore, we particularly welcome articles that unravel new molecular aspects of redox-regulated functions during innate immune responses. Articles that offer novel methodological approaches for detailed analysis of ROS production in innate immune cells are also highly appreciated.

Dr. Marc Herb
Prof. Dr. Roberto Giovannoni
Guest Editors

Manuscript Submission Information

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Keywords

  • reactive oxygen species
  • NADPH oxidase (Nox)
  • mitochondria
  • innate immunity
  • redox signaling
  • infection
  • inflammation

Published Papers (1 paper)

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Research

18 pages, 1864 KiB  
Article
MARCKS Is an Essential Regulator of Reactive Oxygen Species Production in the Monocytic Cell Type
by René Huber, Mareike Diekmann, Leonie Hoffmeister, Friederike Kühl, Bastian Welz and Korbinian Brand
Antioxidants 2022, 11(8), 1600; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11081600 - 18 Aug 2022
Cited by 1 | Viewed by 1625
Abstract
Myristoylated alanine-rich C-kinase substrate (MARCKS) is a ubiquitous protein mediating versatile effects in a variety of cell types, including actin crosslinking, signal transduction, and intracellular transport processes. MARCKS’s functional role in monocyte/macrophages, however, has not yet been adequately addressed. Thus, the aim of [...] Read more.
Myristoylated alanine-rich C-kinase substrate (MARCKS) is a ubiquitous protein mediating versatile effects in a variety of cell types, including actin crosslinking, signal transduction, and intracellular transport processes. MARCKS’s functional role in monocyte/macrophages, however, has not yet been adequately addressed. Thus, the aim of this study was to further elucidate the impact of MARCKS on central cellular functions of monocytic cells. To address this topic, we generated monocytic THP-1 (Tohoku Hospital Pediatrics-1)-derived MARCKS wildtype and knockout (KO) cells using the CRISPR/Cas9 technique. Remarkably, in the absence of MARCKS, both total and intracellular reactive oxygen species (ROS) production were strongly suppressed but restored following transient MARCKS re-transfection. In contrast, proliferation, differentiation, cytokine expression, and phagocytosis remained unaltered. A complete inhibition of ROS production could also be achieved in THP-1-derived PKCβ KO cells or in PKC inhibitor Staurosporine-treated primary human monocytes. MARCKS deficiency also involved reduced basal Akt phosphorylation and delayed re-phosphorylation. Further analyses indicated that long-term TNF pre-incubation strongly enhances monocytic ROS production, which was completely blocked in MARCKS and PKCβ KO cells. Collectively, our study demonstrates that MARCKS is an essential molecule enabling ROS production by monocytic cells and suggests that MARCKS is part of a signal cascade involved in ROS formation. Full article
(This article belongs to the Special Issue The Role of Reactive Oxygen Species in Innate Immunity)
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