Reactive Oxygen Species in the Immune System

Yang, Yuhui; Bazhin, Alexandr V.; Werner, Jens; Karakhanova, Svetlana

doi:10.3109/08830185.2012.755176

Cited by 420 publications

(311 citation statements)

References 157 publications

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“…Depressed production of various cytokines by immune cells (macrophages, neutrophils, lymphocytes) in broilers as a result of arsenic toxicity was previously reported by Khan et al (2014). This decrease in production of cytokines/chemokines (and other immune parameter changes) could be a response to an increased production of reactive oxygen and reactive nitrogen species (ROS and RNS) in response to the arsenic (Yang et al 2013). Induction of oxidative stress has long been considered a mode of toxic action for arsenic.…”

Section: Discussionmentioning

confidence: 99%

Immunosuppressive effects of arsenic in broiler chicks exposed to Newcastle disease virus

Sattar

Khan

Hussain

et al. 2016

Journal of Immunotoxicology

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To assess the effects of prolonged exposure to arsenic (As, as arsenate) on host immune competence overall and resistance to Newcastle disease (ND) viral infection in particular, a study was carried out in broiler chicks. At 7 days of age, chicks were assigned to groups that would undergo varying vaccination, challenge, and/or As exposures; Group 1 was a control; Group 2 was to receive Newcastle disease virus (NDV) only; two groups (Groups 3, 4) were to be given As daily (50 mg/kg, by gavage) from Days 7-35 of the experiment. All groups underwent normal vaccination on Days 5, 23, and 32 against live NDV (B1 type, LaSota strain); two groups (Groups 2, 4) were challenged with field-isolated NDV at Day 24. At Days 14, 21, 28, and 35 of age, subsets of chicks in each group were evaluated. The results showed feed intake and weight gain were lower in As-treated and NDV-challenged chicks. In As-treated chicks, absolute and relative spleen weights were significantly greater, whereas those of the thymus significantly lower, over the entire 35-day period. Effects on bursa weights (absolute, relative) were only significantly reduced through Day 21. Antibody titers against ND were significantly reduced (vs. control) over the whole 35 days in birds that received As alone, but only significantly depressed through the first 21 days in birds that received As þ NDV; thereafter, titers were significantly greater (in parallel with effects in birds that received NDV alone). In contrast, antibody responses to T-dependent antigen (Sheep red blood cells [SRBC]) were significantly lower in As only-and As þ NDV-treated chicks throughout the study period. Among birds exposed to As (alone or with NDV), in situ phagocytic activity was elevated and cutaneous sensitivity responses decreased during the period from Day 28 to Day 35. NDV alone had spurious effects on phagocytic activity but did cause significant reductions in cutaneous sensitivity responses. It was concluded that arsenic decreased immunity in broiler chicks, thereby making them prone to ND. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Immunosuppressive effects of arsenic in broiler chicks exposed to Newcastle disease virus

Sattar

Khan

Hussain

et al. 2016

Journal of Immunotoxicology

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“…ROS regulate a wide range of biological processes, including oxygen sensing, immune responses, cell proliferation and differentiation (42,43). The direct or indirect accumulation of ROS lead to apoptosis (44).…”

Section: Discussionmentioning

confidence: 99%

Targeted inhibition of mitochondrial Hsp90 induces mitochondrial elongation in Hep3B hepatocellular carcinoma cells undergoing apoptosis by increasing the ROS level

Yoo

Kim

Rho

et al. 2015

International Journal of Oncology

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Abstract. Previous studies reported that a Gamitrinib variant containing triphenylphosphonium (G-TPP) binds to mitochondrial Hsp90 and rapidly inhibits its activity to induce apoptosis. We investigated the mechanisms underlying the antitumor activity of G-TPP in Hep3B hepatocellular carcinoma cells. Contrary to our predictions, we observed mitochondrial elongation in the G-TPP-treated Hep3B cells undergoing apoptosis. We found that the G-TPP-induced mitochondrial elongation in Hep3B cells was caused by a decrease in the mitochondrial fission-regulating protein Drp1 rather than by changes in the mitochondrial fusion machinery proteins Mfn1 and Opa1. Furthermore, G-TPP induced G2-M phase cell cycle arrest by reducing the interaction between CDK1 and cyclin B1. Additionally, reactive oxygen species (ROS) played a pivotal role in G-TPP-induced cell death and mitochondrial elongation in Hep3B cells, and these processes are mediated by the reduced association of CDK1 with cyclin B1 and the suppressed phosphorylation of Drp1 (Ser616). Thus, G-TPP induces cell death and causes Drp1-mediated mitochondrial elongation in Hep3B cells by increasing the ROS level.

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“…in the ribosomal genes, the most frequent oxidative DNA adducts are 8-oxodG 95 , however, thymine glycol is also frequent 96,97 . Additional mtDNA lesions include abasic sites (from OH*-mediated hydrolysis), cytosine alkylation by S-adenosylmethionine (SAM) 95 , replication-mediated mismatch of modified nucleotides 98 and repair-or replicationinduced SSBs 99 or DSBs 100 [12]. Abundant expression of mitochondrial NO* and secondary radicals are also responsible for mtDNA damage.…”

Section: Mtdna Damagementioning

confidence: 99%

“…However, ROS, as well as the more stable and less reactive by-product of ROS production, hydrogen-peroxide (H 2 O 2 ), are more than toxic products of respiratory burst, they are also effectors for a plethora of signalling pathways inducing innate and adaptive immune cell recruitment, proliferation, tissue healing, cell survival or apoptosis [12][13][14] . As a secondary messenger ROS are essential contributors to the signalling cascade of receptors (e.g.…”

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confidence: 99%

Inflammation-induced DNA damage and damage-induced inflammation: a vicious cycle

Pálmai-Pallag

Bachrati

2014

Microbes and Infection

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Inflammation is the ultimate response to the constant challenges of the immune system by microbes, irritants or injury. The inflammatory cascade initiates with the recognition of microorganism-derived pathogen associated molecular patterns (PAMPs) and host cell-derived damage associated molecular patterns (DAMPs) by the pattern recognition receptors (PRRs). DNA as a molecular PAMP or DAMP is sensed directly or via specific binding proteins to instigate proinflammatory response. Some of these DNA binding proteins also participate in canonical DNA repair pathways and recognise damaged DNA to initiate DNA damage response. In this review we aim to capture the essence of the complex interplay between DNA damage response and the proinflammatory signalling through representative examples. Aetiology and molecular consequences of inflammationInflammation, from the latin inflammare: set on fire, in mammals is the natural defence mechanism of the immune system in response to the constant challenges it is exposed to including injury, toxins and microorganisms, low level cosmic or medical quality radiations (X-ray, -irradiation or UVA/B), drugs and air pollutants (e.g. asbestos or cigarette smoke) 1,2 *. Inflammation is a hallmark of aging and many chronic diseases such as obesity, Chron's disease, Parkinson's disease and autoimmune diseases just to name a few [3][4][5][6][7] . *Additional on-line references are marked by superscript numbers 3The first phase of a complex defence mechanism is acute inflammation instigated by the infiltrated peripheral polymorphonuclear leukocytes (neutrophils), granulocytes (eosinophils) and tissue resident phagocytes (macrophages) at the site of insult. The pro-inflammatory signal is transmitted through the PRRs that can identify danger through DAMPs (e.g. ROS, circulating DNA fragments), cytokines or chemokines released by the damaged tissue or PAMPs from pathogens [1] 8 . The initial role of these cells is to remove the invading pathogen and initiate tissue repair 9 .One of the major defence mechanisms of the activated neutrophils and macrophages is the production of a vast spectrum of endogenous reactive oxygen (ROS) and nitrogen (RNS) species 10 in a process termed "respiratory burst" 11 (see below). However, ROS, as well as the more stable and less reactive by-product of ROS production, hydrogen-peroxide (H 2 O 2 ), are more than toxic products of respiratory burst, they are also effectors for a plethora of signalling pathways inducing innate and adaptive immune cell recruitment, proliferation, tissue healing, cell survival or apoptosis [12][13][14] . Generation of inflammation-induced ROS and RNS mtDNA damageThe circular mtDNA constitutes 1% of total cellular DNA, is of symbiotic bacterial origin, and compared to nuDNA has a very different molecular organisation and regulation. mtDNA has no histones and the methylation of CpG repeat motifs is under-represented, therefore it is particularly vulnerable to damage by endogenous ROS generated by the oxidative electron transpor...

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Reactive Oxygen Species in the Immune System

Cited by 420 publications

References 157 publications

Immunosuppressive effects of arsenic in broiler chicks exposed to Newcastle disease virus

Immunosuppressive effects of arsenic in broiler chicks exposed to Newcastle disease virus

Targeted inhibition of mitochondrial Hsp90 induces mitochondrial elongation in Hep3B hepatocellular carcinoma cells undergoing apoptosis by increasing the ROS level

Inflammation-induced DNA damage and damage-induced inflammation: a vicious cycle

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