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      Inhibition of NADPH Oxidase-Derived Reactive Oxygen Species Decreases Expression of Inflammatory Cytokines in A549 Cells

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          Abstract

          Various experimental models strongly support the hypothesis that airway inflammation can be caused by oxidative stress. Inflammatory airway diseases like asthma and COPD are characterized by higher levels of ROS and inflammatory cytokines. One of the sources of ROS is NADPH oxidase. Therefore, the aim of the study was to investigate influence of NADPH oxidase inhibition on the expression of IL-6, IL-8, TNF, TSLP, CD59, and PPAR-γ in vitro. A549 cells were incubated with apocynin in three concentrations (0.5 mg/ml, 1 mg/ml, and 3 mg/ml). Cells were trypsinized and RNA isolated after 1 h, 2 h, and 4 h of apocynin incubation at each concentration. Afterwards, reverse transcription was performed to evaluate mRNA expression using real-time PCR. The time-response and dose-response study showed that apocynin significantly influenced the relative expression of chosen genes ( IL-6, IL-8, TNF, PPAR-γ, TSLP, and CD59). Apocynin decreased the mRNA expression of TNF-α at all concentrations used, and of IL-6 at concentrations of 1 and 3 mg/ml ( p < 0.05). TSLP mRNA expression was also reduced by apocynin after 1 h and 2 h, and CD59 mRNA after 1 h, but only at the highest concentration. The expression of PPAR-γ was reduced after apocynin in the highest concentrations only ( p < 0.05). The results might suggest that proinflammatory agents’ expression levels are strongly connected to the presence of oxidative stress generated by NADPH oxidase and this might be at least partially eliminated by anti-oxidative action. Apocynin, as an effective inhibitor of NADPH oxidase, seems to be useful in potential anti-oxidative and anti-inflammatory therapy.

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          Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis.

          Individuals with chronic obstructive pulmonary disease (COPD) are at increased risk of cardiovascular diseases, osteoporosis, and muscle wasting. Systemic inflammation may be involved in the pathogenesis of these disorders. A study was undertaken to determine whether systemic inflammation is present in stable COPD. A systematic review was conducted of studies which reported on the relationship between COPD, forced expiratory volume in 1 second (FEV(1)) or forced vital capacity (FVC), and levels of various systemic inflammatory markers: C-reactive protein (CRP), fibrinogen, leucocytes, tumour necrosis factor-alpha (TNF-alpha), and interleukins 6 and 8. Where possible the results were pooled together to produce a summary estimate using a random or fixed effects model. Fourteen original studies were identified. Overall, the standardised mean difference in the CRP level between COPD and control subjects was 0.53 units (95% confidence interval (CI) 0.34 to 0.72). The standardised mean difference in the fibrinogen level was 0.47 units (95% CI 0.29 to 0.65). Circulating leucocytes were also higher in COPD than in control subjects (standardised mean difference 0.44 units (95% CI 0.20 to 0.67)), as were serum TNF-alpha levels (standardised mean difference 0.59 units (95% CI 0.29 to 0.89)). Reduced lung function is associated with increased levels of systemic inflammatory markers which may have important pathophysiological and therapeutic implications for subjects with stable COPD.
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            Role of NADPH oxidase/ROS in pro-inflammatory mediators-induced airway and pulmonary diseases.

            Reactive oxygen species (ROS) are products of normal cellular metabolism and are known to act as second messengers. Under physiological conditions, ROS participate in maintenance of cellular 'redox homeostasis' in order to protect cells against oxidative stress. In addition, regulation of redox state is important for cell activation, viability, proliferation, and organ function. However, overproduction of ROS, most frequently due to excessive stimulation of either reduced nicotinamide adenine dinucleotide phosphate (NADPH) by pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) or the mitochondrial electron transport chain and xanthine oxidase, results in oxidative stress. Oxidative stress is a deleterious process that leads to airway and lung damage and consequently to several respiratory inflammatory diseases/injuries, including acute respiratory distress syndrome (ARDS), asthma, cystic fibrosis (CF), and chronic obstructive pulmonary disease (COPD). Many of the known inflammatory target proteins, such as matrix metalloproteinase-9 (MMP-9), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A(2) (cPLA(2)), are associated with NADPH oxidase activation and ROS overproduction in response to pro-inflammatory mediators. Thus, oxidative stress regulates both key inflammatory signal transduction pathways and target proteins involved in airway and lung inflammation. In this review, we discuss mechanisms of NADPH oxidase/ROS in the expression of inflammatory target proteins involved in airway and lung diseases. Knowledge of the mechanisms of ROS regulation could lead to the pharmacological manipulation of antioxidants in airway and lung inflammation and injury. Copyright © 2012 Elsevier Inc. All rights reserved.
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              Thymic stromal lymphopoietin expression is increased in asthmatic airways and correlates with expression of Th2-attracting chemokines and disease severity.

              Thymic stromal lymphopoietin (TSLP) is said to increase expression of chemokines attracting Th2 T cells. We hypothesized that asthma is characterized by elevated bronchial mucosal expression of TSLP and Th2-attracting, but not Th1-attracting, chemokines as compared with controls, with selective accumulation of cells bearing receptors for these chemokines. We used in situ hybridization and immunohistochemistry to examine the expression and cellular provenance of TSLP, Th2-attracting (thymus and activation-regulated chemokine (TARC)/CCL17, macrophage-derived chemokine (MDC)/CCL22, I-309/CCL1) and Th1-attracting (IFN-gamma-inducible protein 10 (IP-10)/CXCL10, IFN-inducible T cell alpha-chemoattractant (I-TAC)/CXCL11) chemokines and expression of their receptors CCR4, CCR8, and CXCR3 in bronchial biopsies from 20 asthmatics and 15 normal controls. The numbers of cells within the bronchial epithelium and submucosa expressing mRNA for TSLP, TARC/CCL17, MDC/CCL22, and IP-10/CXCL10, but not I-TAC/CXCL11 and I-309/CCL1, were significantly increased in asthmatics as compared with controls (p
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                Author and article information

                Contributors
                +48 (42) 272 53 01 , rafal.pawliczak@csk.umed.lodz.pl
                Journal
                Inflammation
                Inflammation
                Inflammation
                Springer US (New York )
                0360-3997
                1573-2576
                14 October 2019
                14 October 2019
                2019
                : 42
                : 6
                : 2205-2214
                Affiliations
                [1 ]GRID grid.8267.b, ISNI 0000 0001 2165 3025, Department of Immunopathology, , Medical University of Lodz, ; 7/9 Zeligowskiego, Bldg 2, Rm 122, 90-752 Lodz, Poland
                [2 ]GRID grid.8267.b, ISNI 0000 0001 2165 3025, Department of Biology and Pharmaceutical Botany, , Medical University of Lodz, ; Lodz, Poland
                [3 ]GRID grid.10789.37, ISNI 0000 0000 9730 2769, Department of Genetics and Plant Molecular Biology and Biotechnology, , The University of Lodz, ; Lodz, Poland
                Article
                1084
                10.1007/s10753-019-01084-0
                6856491
                31612365
                ab27935d-e1d7-4b82-9be8-09712c37ef4a
                © The Author(s) 2019

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100005888, Uniwersytet Medyczny w Lodzi;
                Award ID: 503/0-148-03/503-01
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100004281, Narodowe Centrum Nauki;
                Award ID: 2015/19/D/NZ6/02988
                Award Recipient :
                Categories
                Original Article
                Custom metadata
                © Springer Science+Business Media, LLC, part of Springer Nature 2019

                Immunology
                inflammatory cytokines,oxidative stress,apocynin
                Immunology
                inflammatory cytokines, oxidative stress, apocynin

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