Reactive Oxygen Species (ROS) Signaling and Immune Diseases.

Editorial

21 May 2024

Editorial: Reactive oxygen species signaling and immune diseases

Saikolappan Sankaralingam

and

Gopi Kolluru

948 views

1 citations

Editors

SAIKOLAPPAN SANKARALINGAM

Ramkumar Thiyagarajan

University of Kansas Medical Center

Impact

Review

07 March 2024

ROS signaling in innate immunity via oxidative protein modifications

Renuka Ramalingam Manoharan

, 2 more and

Julia Kzhyshkowska

Superoxide (O2•-) generated by NOX or mitochondrial electron transfer chain is converted into H2O2 by superoxide dismutase (SOD), which balance between both pro-inflammatory (M1) and anti-inflammatory (M2) response of macrophage during polarization events. The figure was Created with BioRender.com.

The innate immune response represents the first-line of defense against invading pathogens. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have been implicated in various aspects of innate immune function, which involves respiratory bursts and inflammasome activation. These reactive species widely distributed within the cellular environment are short-lived intermediates that play a vital role in cellular signaling and proliferation and are likely to depend on their subcellular site of formation. NADPH oxidase complex of phagocytes is known to generate superoxide anion radical (O₂^•−) that functions as a precursor for antimicrobial hydrogen peroxide (H₂O₂) production, and H₂O₂ is utilized by myeloperoxidase (MPO) to generate hypochlorous acid (HOCl) that mediates pathogen killing. H₂O₂ modulates the expression of redox-responsive transcriptional factors, namely NF-kB, NRF2, and HIF-1, thereby mediating redox-based epigenetic modification. Survival and function of immune cells are under redox control and depend on intracellular and extracellular levels of ROS/RNS. The current review focuses on redox factors involved in the activation of immune response and the role of ROS in oxidative modification of proteins in macrophage polarization and neutrophil function.

7,899 views

28 citations

(A) Dot plots with histograms representing ROS production in B-cell subpopulations from a representative control and CVID patient. (i) Gating strategy: viable B cells were selected based on forward and side scatter, non-expression of SYTOX marker, and CD19+ expression. B-cell subpopulations were identified as naïve CD19+CD27− (green color) and memory CD19+CD27+ (purple color). (ii) ROS production was identified as the percentage of cells positive for CellROX Deep Red probe (% CellROX+ cells). Histograms show the percentage (upper right corner) of ROS-producing cells from healthy control (left histograms) and CVID patients (right histograms). (B) Comparison between the percentages of CellROX+ naïve CD19+CD27− (green dots) and memory CD19+CD27+ (purple dots) B cells from (i) healthy controls and (i) CVID patients after 24 h of culture without or with stimulation with anti-BCR, anti-CD40, CpG-ODN, anti-BCR+IL-21, anti-CD40+IL-21, anti-BCR+CpG-ODN, or anti-BCR+anti-CD40. (C) Percentages of unstimulated CellROX+ naïve CD19+CD27− (green dots) and memory CD19+CD27+ (purple dots) from healthy controls (empty dots) and CVID patients (filled dots). (B, C) Each dot represents an individual; black horizontal lines illustrate the median of the group. Mann–Whitney test p-values: ****p < 0.0001.

Original Research

26 March 2024

Dysfunctional mitochondria, disrupted levels of reactive oxygen species, and autophagy in B cells from common variable immunodeficiency patients

Maria Berman-Riu

, 4 more and

Joana M. Ferrer

2,702 views

0 citations

Review

25 May 2023

Reactive oxygen species formation and its effect on CD4+ T cell-mediated inflammation

Panyin Shu

, 4 more and

Dunfang Zhang

5,459 views

15 citations

Simplified figure depicting various possible mechanisms of TAMs associated with ROS at a cellular-level affect oncogenesis and development of tumor in TME.

Review

21 July 2023

Targeting reactive oxygen species and fat acid oxidation for the modulation of tumor-associated macrophages: a narrative review

Yujian Teng

, 4 more and

Ming Liu

4,585 views

7 citations

Original Research

31 May 2023

Development of innate immune memory by non-immune cells during Staphylococcus aureus infection depends on reactive oxygen species

Emmanuel Chaumond

, 7 more and

Nadia Berkova

3,798 views

2 citations

Opinion

20 February 2024

Exploring the ROS reduction strategies in chronic lupus management

Kannika Parameshwari Kannan

and

Smiline Girija A.S.

1,807 views

1 citations

Review

29 April 2022

Reactive Oxygen Species Induce Fatty Liver and Ischemia-Reperfusion Injury by Promoting Inflammation and Cell Death

Shen-ping Tang

, 4 more and

Shao-wei Li

Liver transplantation is the ultimate method for treating end-stage liver disease. With the increasing prevalence of obesity, the number of patients with non-alcoholic fatty liver, a common cause of chronic liver disease, is on the rise and may become the main cause of liver transplantation in the future. With the increasing gap between the number of donor livers and patients waiting for liver transplantation and the increasing prevalence of non-alcoholic fatty liver, the proportion of steatosis livers among non-standard donor organs is also increasing. Ischemia-reperfusion injury has historically been the focus of attention in the liver transplantation process, and severe ischemia-reperfusion injury leads to adverse outcomes of liver transplantation. Studies have shown that the production of reactive oxygen species and subsequent oxidative stress play a key role in the pathogenesis of hepatic ischemia and reperfusion injury and non-alcoholic fatty liver. Furthermore, the sensitivity of fatty liver transplantation to ischemia-reperfusion injury has been suggested to be related to the production of reactive oxygen species (ROS) and oxidative stress. In ischemia-reperfusion injury, Kupffer cell and macrophage activation along with mitochondrial damage and the xanthine/xanthine oxidase system promote marked reactive oxygen species production and the inflammatory response and apoptosis, resulting in liver tissue injury. The increased levels of ROS and lipid peroxidation products, vicious circle of ROS and oxidative stress along with mitochondrial dysfunction promoted the progress of non-alcoholic fatty liver. In contrast to the non-fatty liver, a non-alcoholic fatty liver produces more reactive oxygen species and suffers more serious oxidative stress when subjected to ischemia-reperfusion injury. We herein review the effects of reactive oxygen species on ischemia-reperfusion injury and non-alcoholic fatty liver injury as well as highlight several treatment approaches.

10,027 views

105 citations