Ionizing radiation promotes CCL27 secretion from keratinocytes through the cross talk between TNF‐α and ROS

Zhang, Qian; Zhu, Linlin; Wang, Gang; Zhao, Ye; Xiong, Na; Bao, Hegang; Jin, Wei

doi:10.1002/jbt.21868

Cited by 15 publications

(15 citation statements)

References 31 publications

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“…Our study found a positive correlation between serum levels of CCL27 and TNF-α during the acute stage. Several studies have shown that TNF-α can induce keratinocytes to secrete CCL27 in vitro [ 13 , 32 ]. Taking these findings into account, we hypothesized that the keratinocytes amplify inflammation in SJS/TEN.…”

Section: Discussionmentioning

confidence: 99%

Diverse expression of TNF-α and CCL27 in serum and blister of Stevens–Johnson syndrome/toxic epidermal necrolysis

Wang

Luo

et al. 2018

Clin Transl Allergy

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BackgroundThe pathogenesis of Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) is not fully understood. Our previous study reported that chemokine CCL27 was overexpressed in serum of SJS/TEN patients. The objective of this study was to investigate the levels of CCL27 and TNF-α in serum and blister fluid from patients with SJS/TEN during the acute stage or resolution phase.MethodsA total of 27 patients with SJS/TEN and 39 healthy donors were recruited to the study. Serum and vesicular levels of CCL27 and TNF-α were determined by enzyme-linked immunosorbent assays.ResultsSerum levels of CCL27 and TNF-α were significantly elevated in patients with SJS/TEN during the acute stage as compared to the resolution phase and also compared with levels observed in normal controls (P = 0.001/< 0.001; P = 0.012/< 0.001). Serum TNF-α levels were significantly higher in patients with SJS/TEN during the resolution phase compared with normal controls (P < 0.001). Serum CCL27 levels were positively correlated with TNF-α levels during the acute stage (rs = 0.660; P < 0.001). Blister fluid exhibited much lower CCL27 levels than serum did during the acute stage (P = 0.008). TNF-α levels were much higher in vesicles in contrast to serum from acute stage (P = 0.040) as well as serum from resolution phase (P = 0.029).ConclusionsOur study demonstrated roles of CCL27 and TNF-α in promoting the course of SJS/TEN. CCL27 may act early in the course of disease, via the circulation, whereas TNF-α acts throughout the course of disease, in skin lesions.

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Section: Discussionmentioning

confidence: 99%

Diverse expression of TNF-α and CCL27 in serum and blister of Stevens–Johnson syndrome/toxic epidermal necrolysis

Wang

Luo

et al. 2018

Clin Transl Allergy

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“…RONS levels increase at multiple time points in vitro and in vivo following IR indicating a persistent effect (Fig. 2) (Ameziane- El-Hassani et al 2015;Choi et al 2007;Das et al 2014;Datta et al 2012b;Denissova et al 2012;Du et al 2009;Lyng et al 2001;Manna et al 2015;Martin et al 2014;Narayanan et al 1997;Pazhanisamy et al 2011;Saenko et al 2013;Werner et al 2014;Yang et al 2005;Yoshida et al 2012;Zhang et al 2017). Ionizing radiation initially generates RONS by direct hydrolysis of water molecules.…”

Section: Evidence Of Activation By Irmentioning

confidence: 99%

“…Similarly, decreased antioxidant activity and higher RONS are observed in cells with GI (Bensimon et al 2016;Buonanno et al 2011;Datta et al 2012b;Dayal et al 2008;Kim et al 2006;Natarajan et al 2007;Owens et al 2012;Pazhanisamy et al 2011;Thomas et al 2012). RONS are also involved in the activation of inflammation (Nakao et al 2008;Zhang et al 2017) and epigenetic effects (Bernal et al 2013;Galligan et al 2014;Kloypan et al 2015;Simone et al 2009;Yang et al 2014).…”

Section: Essentiality Of Ronsmentioning

confidence: 99%

“…The strongest evidence for the essentiality of RONS in breast cancer from IR comes from studies, showing that reducing RONS with antioxidants including catalase or SOD or NOX/DUOX inhibitors also reduces downstream key events including DNA damage and GI in multiple types of irradiated cells and bystander cells in vivo and in vitro after IR (Ameziane- El-Hassani et al 2010Azzam et al 2002;Bensimon et al 2016;Choi et al 2007;Dayal et al 2008Dayal et al , 2009Douki et al 2006;Jones et al 2007;Manna et al 2015;Ozyurt et al 2014;Pazhanisamy et al 2011;Tartier et al 2007;Tian et al 2015;Weyemi et al 2015;Winyard et al 1992;Yang et al 2007bYang et al , 2005, while inhibiting NO in particular inhibits DNA damage and mutations in bystander cells (Han et al 2010;Tartier et al 2007;Yang et al 2007b;Zhou et al 2008). Antioxidant activity also reduces the inflammatory response to IR in animals and cultured skin cells (Berruyer et al 2004;Das et al 2014;Ezz et al 2018;Haddadi et al 2017;Khan et al 2015;Ozyurt et al 2014;Sinha et al 2011Sinha et al , 2012Zetner et al 2016;Zhang et al 2017) and the epigenetic effects of IR in vitro (Bernal et al 2013;Kloypan et al 2015;Simone et al 2009). RONS also drives proliferation directly (Han et al 2010) and via cell death and compensatory proliferation following damage to DNA and important cellular macromolecule...…”

Section: Essentiality Of Ronsmentioning

confidence: 99%

“…One mechanism of cancer promotion involves oxidative activity and DNA damage: inflammation in response to IR increases oxidative activity in a positive feedback loop leading to increased DNA lesions, GI, and mutations. Oxidative activity mediates the increase in inflammatory (TNF-α and neutrophil) markers (Ozyurt et al 2014), and oxidative activity is increased by direct treatment with TNF-α or neutrophils (Jackson et al 1989;Natarajan et al 2007;Yan et al 2006;Yang et al 2007a) or after IR mediated by Il13, TNF-α, CCL2, COX2, and TLR9 (Ameziane- El-Hassani et al 2015;Jackson et al 1989;Kostyuk et al 2012;Redon et al 2010;Stevens et al 1992;Zhang et al 2017). Cytokines IL13 and TNF-α, neutrophils, and COX2 damage DNA and increase mutations indirectly in IR cells (Ameziane-El-Hassani et Bisht et al 2003;Burr et al 2010;Hosseinimehr et al 2015;Jackson et al 1989;Ozyurt et al 2014;Yan et al 2006), and NO, TGF-β, NF-kβ, and COX2 increase DNA damage and mutations in bystander cells (Chai et al 2013b;Dickey et al 2009;Han et al 2010;Redon et al 2010;Shao et al 2008;Zhou et al 2005;Zhou et al 2008).…”

Section: Essentiality Of Inflammationmentioning

confidence: 99%

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Adverse outcome pathways for ionizing radiation and breast cancer involve direct and indirect DNA damage, oxidative stress, inflammation, genomic instability, and interaction with hormonal regulation of the breast

Helm

Rudel

2020

Arch Toxicol

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Knowledge about established breast carcinogens can support improved and modernized toxicological testing methods by identifying key mechanistic events. Ionizing radiation (IR) increases the risk of breast cancer, especially for women and for exposure at younger ages, and evidence overall supports a linear dose-response relationship. We used the Adverse Outcome Pathway (AOP) framework to outline and evaluate the evidence linking ionizing radiation with breast cancer from molecular initiating events to the adverse outcome through intermediate key events, creating a qualitative AOP. We identified key events based on review articles, searched PubMed for recent literature on key events and IR, and identified additional papers using references. We manually curated publications and evaluated data quality. Ionizing radiation directly and indirectly causes DNA damage and increases production of reactive oxygen and nitrogen species (RONS). RONS lead to DNA damage and epigenetic changes leading to mutations and genomic instability (GI). Proliferation amplifies the effects of DNA damage and mutations leading to the AO of breast cancer. Separately, RONS and DNA damage also increase inflammation. Inflammation contributes to direct and indirect effects (effects in cells not directly reached by IR) via positive feedback to RONS and DNA damage, and separately increases proliferation and breast cancer through pro-carcinogenic effects on cells and tissue. For example, gene expression changes alter inflammatory mediators, resulting in improved survival and growth of cancer cells and a more hospitable tissue environment. All of these events overlap at multiple points with events characteristic of "background" induction of breast carcinogenesis, including hormone-responsive proliferation, oxidative activity, and DNA damage. These overlaps make the breast particularly susceptible to ionizing radiation and reinforce that these biological activities are important characteristics of carcinogens. Agents that increase these biological processes should be considered potential breast carcinogens, and predictive methods are needed to identify chemicals that increase these processes. Techniques are available to measure RONS, DNA damage and mutation, cell proliferation, and some inflammatory proteins or processes. Improved assays are needed to measure GI and chronic inflammation, as well as the interaction with hormonally driven development and proliferation. Several methods measure diverse epigenetic changes, but it is not clear which changes are relevant to breast cancer. In addition, most toxicological assays are not conducted in mammary tissue, and so it is a priority to evaluate if results from other tissues are generalizable to breast, or to conduct assays in breast tissue. Developing and applying these assays to identify exposures of concern will facilitate efforts to reduce subsequent breast cancer risk.Biological systems studied This review article summarizes and synthesizes data from cell-culture, experimental animals, and human epidem...

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CCL27 Signaling in the Tumor Microenvironment

Martínez‐Rodríguez

Monteagudo

2021

Advances in Experimental Medicine and Biology

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Ionizing radiation promotes CCL27 secretion from keratinocytes through the cross talk between TNF‐α and ROS

Cited by 15 publications

References 31 publications

Diverse expression of TNF-α and CCL27 in serum and blister of Stevens–Johnson syndrome/toxic epidermal necrolysis

Diverse expression of TNF-α and CCL27 in serum and blister of Stevens–Johnson syndrome/toxic epidermal necrolysis

Adverse outcome pathways for ionizing radiation and breast cancer involve direct and indirect DNA damage, oxidative stress, inflammation, genomic instability, and interaction with hormonal regulation of the breast

CCL27 Signaling in the Tumor Microenvironment

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