Review – Mediators of Asthma Series
Reactive Oxygen Species as Mediators in Asthma

https://doi.org/10.1006/pupt.2001.0319Get rights and content

Abstract

This review describes production and effects of reactive oxygen species (ROS) on airway function. ROS are important in many physiological processes but can also have detrimental effects on airway cells and tissues when produced in high quantities or during the absence of sufficient amounts of anti-oxidants. Therefore, these mediators play a prominent role in the pathogenesis of various inflammatory airway disorders, including asthma. Effects of ROS on airway function in asthma have been studied with isolated airway cells and tissues and with animal models and patients. With the use of inhibitors, transgenic animals and measurements of the release of ROS within the airways, it became clear that oxidative stress contributes to the initiation and worsening of inflammatory respiratory disorders.

References (183)

  • LJ Janssen

    Isoprostanes: generation, pharmacology, and roles in free-radical-mediated effects in the lung

    Pulm Pharmacol Ther

    (2000)
  • JD Morrow et al.

    The isoprostanes. Current knowledge and directions for future research

    Biochem Pharmacol

    (1996)
  • KK Griendling et al.

    Redox control of vascular smooth muscle proliferation

    J Lab Clin Med

    (1998)
  • IM Adcock et al.

    Oxidative stress induces NFκB DNA binding and inducible NOS mRNA in human epithelial cells

    Biochem Biophys Res Commun

    (1994)
  • JJ Haddad et al.

    Antioxidant/pro-oxidant equilibrium regulates HIF-1α and NF-κB redox sensitivity. Evidence for inhibition by glutathione oxidation in alveolar epithelial cells

    J Biol Chem

    (2000)
  • PAJ Henricks et al.

    Pharmacological modulation of cell adhesion molecules

    Eur J Pharmacol

    (1998)
  • I Rahman

    Regulation of nuclear-factor-κB, activator protein-1, and glutathione levels by tumor necrosis factor-α and dexamethasone in alveolar epithelial cells

    Biochem Pharmacol

    (2000)
  • A Fraticelli et al.

    Hydrogen peroxide and superoxide modulate leukocyte adhesion molecule expression and leukocyte endothelial adhesion

    Biochim Biophys Acta

    (1996)
  • CV Serrano et al.

    Superoxide and hydrogen peroxide induce CD18-mediated adhesion in the postischemic heart

    Biochim Biophys Acta

    (1996)
  • D Raeburn

    Eicosanoids, epithelium and airway reactivity

    Gen Pharmacol

    (1990)
  • H Bayram et al.

    Effect of ozone and nitrogen dioxide on the release of proinflammatory mediators from bronchial epithelial cells of non-atopic non-asthmatic subjects and atopic asthmatic patients in vitro

    J Allergy Clin Immunol

    (2001)
  • JE Repine et al.

    Oxidative stress in chronic obstructive pulmonary disease

    Am J Respir Crit Care Med

    (1997)
  • V Vallyathan et al.

    The role of oxygen free radicals in occupational and environmental lung diseases

    Environ Health Perspect

    (1997)
  • BM Babior et al.

    Biological defense mechanisms. The production by leukocytes of superoxide, a potential bactericidal agent

    J Clin Invest

    (1973)
  • PAJ Henricks et al.

    Modulation of phagocytic cell function

    Vet Res Commun

    (1986)
  • SA Jones et al.

    Expression of phagocyte NADPH oxidase components in human endothelial cells

    Am J Physiol

    (1996)
  • C Marshall et al.

    Pulmonary artery NADPH-oxidase is activated in hypoxic pulmonary vasoconstriction

    Am J Respir Cell Mol Biol

    (1996)
  • G Sadeghi-Hashjin et al.

    Peroxynitrite in airway diseases

    Clin Exp Allergy

    (1998)
  • MT Krishna et al.

    Toxicological mechanisms underlying oxidant pollutant-induced airway injury

    Rev Environ Health

    (1998)
  • AM Babior

    Oxygen-dependent microbial killing by phagocytes (two parts)

    New Engl J Med

    (1978)
  • SJ Klebanoff

    A peroxidase-mediated antimicrobial system in leukocytes

    J Clin Invest

    (1967)
  • JS Beckman et al.

    Nitric oxide, superoxide, and peroxynitrite: the good, the bad, and the ugly

    Am J Physiol

    (1996)
  • TM Asikainen et al.

    Expression and development profile of antioxidant enzymes in human lung and liver

    Am J Respir Cell Mol Biol

    (1998)
  • AM Cantin et al.

    Antioxidant macromolecules in the epithelial lining fluid of the normal human lower respiratory tract

    J Clin Invest

    (1990)
  • R Exner et al.

    Therapeutic potential of glutathione

    Wien Klin Wochenschr

    (2000)
  • VL Kinnula et al.

    Primary and immortalized (BEAS 2B) human bronchial epithelial cells have significant antioxidative capacity in vitro

    Am J Respir Cell Mol Biol

    (1994)
  • P Pietarinen-Runtti et al.

    Expression of antioxidant enzymes in human inflammatory cells

    Am J Physiol

    (2000)
  • AM Cantin et al.

    Normal alveolar epithelial lining fluid contains high levels of glutathione

    J Appl Physiol

    (1987)
  • AM Cantin

    Taurine modulation of hypochlorous acid-induced lung epithelial cell injury in vitro. Role of anion transport

    J Clin Invest

    (1993)
  • CE Cross et al.

    Oxidative stress and antioxidants at biosurfaces: plants, skin, and respiratory tract surfaces

    Environ Health Perspect

    (1998)
  • R Slade et al.

    Comparison of antioxidant substances in bronchoalveolar lavage cells and fluid from humans, guinea pigs, and rats

    Exp Lung Res

    (1993)
  • DT Wright et al.

    Interactions of oxygen radicals with airway epithelium

    Environ Health Perspect

    (1994)
  • KJ Rhoden et al.

    Effect of hydrogen peroxide on guinea-pig tracheal smooth muscle in vitro: role of cyclo-oxygenase and airway epithelium

    Brit J Pharmacol

    (1989)
  • MK Abe et al.

    Hydrogen peroxide stimulates mitogen-activated protein kinase in bovine tracheal myocytes: implications for human disease

    Am J Respir Cell Mol Biol

    (1994)
  • JL Szarek et al.

    Hydrogen peroxide-induced potentiation of contractile responses in isolated rat airways

    Am J Physiol

    (1990)
  • U Katsumata et al.

    Oxygen radicals produce airway constriction and hyperresponsiveness in anesthetized cats

    Am Rev Respir Dis

    (1990)
  • K Prasad et al.

    Influence of hydroxyl radical on rabbit airway smooth muscle chronically exposed to H2O2in vivo

    Am J Physiol

    (1993)
  • T Asano et al.

    Role of the epithelium in opposing H2O2-induced modulation of acetylcholine-induced contractions in rabbit intrapulmonary bronchiole

    Brit J Pharmacol

    (2001)
  • H Tsukagoshi et al.

    Ozone-induced airway hyperresponsiveness: role of superoxide anions, NEP, and BK receptors

    J Appl Physiol

    (1995)
  • CG Murlas et al.

    HOC1 causes airway substance P hyperresponsiveness and neutral endopeptidase hypoactivity

    Am J Physiol

    (1990)
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      Citation Excerpt :

      AKAPs signal via protein kinase A (PKA) with disruption of AKAP-PKA interactions both augmenting CSE induced IL-8 release from ASM, and diminishing the suppression of this release by formoterol, suggesting that CSE induced changes in AKAP expression could compromise the anti-inflammatory effects of formoterol [117]. ROS are also involved in the down regulation of β-adrenergic signalling [279], which could have implications for the bronchodilatory effects of β-agonists, confounding the effects of ROS on promoting ASM contractility described in this review. In this review we have summarised studies using data from primary airway, bronchial or tracheal smooth muscle cells that assess the role of oxidative stress and ROS in ASM dysfunction relevant to asthma and COPD.

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    Author for correspondence: Paul A. J. Henricks, Department of Pharmacology and Pathophysiology, P.O. Box 80.082, 3508 TB Utrecht, The Netherlands. Tel.: 31-30-2537358 Fax: 31-30-2537420 E-mail: [email protected]

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