Preferences help
enabled [disable] Abstract
Number of results
2009 | 4 | 2 | 245-252
Article title

The production of reactive oxygen species in peripheral blood neutrophils is modulated by airway mucous

Title variants
Languages of publication
Neutrophils are a major source of reactive oxygen species (ROS). The role of airway mucous on ROS production is unknown. The aim of our study was to investigate the direct influence of bronchoalveolar lavage fluid (BALF) and induced sputum (IS) alone or in combination with chemical/biological stimulus on ROS production in peripheral blood neutrophils during chronic obstructive pulmonary disease (COPD). Neutrophils were isolated from peripheral blood of 47 patients with moderate COPD and 14 healthy individuals (HI). BALF/RPMI (1:1) or IS/RPMI (1:1) from COPD patients were used to stimulate neutrophils alone or in combination with phorbolmyristate- acetate (PMA) (0.1–30 nM) or Staphylococcus aureus bacteria (0.7–500 bact/neutrophil). Relative generation of ROS was measured flow cytometrically. BALF/RPMI and in combination with relatively low PMA or all bacteria concentrations stimulated ROS; while, combination with relatively high PMA concentrations suppressed ROS in of COPD patients and HI. IS/RPMI and its combination with PMA inhibited ROS generation in both groups; whereas, IS stimulated or had a tendency to stimulate ROS production with relatively high bacteria concentrations. In conclusion, BALF and IS directly or in combination with chemical/biological factors modulated ROS production. This effect was stronger in neutrophils from COPD patients and depended on chemical/biological stimulus intensity.
BALF   COPD   IS   Neutrophils   ROS  
Physical description
1 - 6 - 2009
27 - 3 - 2009
  • Laboratory of Pulmonology, Institute for Biomedical Research, Kaunas University of Medicine, LT-50009, Kaunas, Lithuania
  • Institute of Immunology, Universtiy of Veterinary Medicine, D-30173, Hannover, Germany
  • Department of Pulmonology and Immunology, Kaunas Medical University Hospital, LT-50009, Kaunas, Lithuania
  • [1] Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease, NHLBI/WHO Workshop Report., 2007,
  • [2] Drost E.M., Skwarski K.M., Sauleda J., Soler N., Roca J., Agusti A., et al., Oxidative stress and airway inflammation in severe exacerbations of COPD, Thorax., 2005, 60, 293–300[Crossref]
  • [3] MacNee W., Airway infection does not accelerate decline in lung function in chronic obstructive pulmonary disease, Am. J. Respir. Crit. Care. Med., 2001, 164, 1758–1760
  • [4] Kulkarni N., Cooke M.S., Grigg J., Neutrophils in induced sputum from healthy children: Role of IL-8 and oxidative stress, Repir. Med., 2007, 101, 2108–2112[Crossref]
  • [5] Noguera A., Batle S., Miralles C., Iglesias J., Busquets X., MacNee W., et al., Enhanced neutrophil response in chronic obstructive pulmonary disease, Thorax, 2001, 56, 432–437[Crossref]
  • [6] Rahman I., Oxidative stress and gene transcription in asthma and chronic obstructive pulmonary disease: antioxidant therapeutic targets, Curr. Drug. Targets. Inflamm. Allergy., 2002, 1, 291–315[Crossref]
  • [7] Repine J.E., Bast A., Lankhorst I., Oxidative stress in chronic obstructive pulmonary disease, Oxidative Stress Study Group, Am. J. Respir. Crit. Care. Med., 1997, 156, 341–357
  • [8] Babusyte A., Stravinskaite K., Jeroch J., Lotvall J., Sakalauskas R., Sitkauskiene B., Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD, Respir Res., 2007, 8, 81[WoS][Crossref]
  • [9] Bowler R.P., Barnes P.J., Crapo J.D., The role of oxidative stress in chronic obstructive pulmonary disease, COPD., 2004, 1, 255–277[Crossref]
  • [10] Keatings V.M., Collins P.D., Scott D.M., Barnes P.J., Differences in interleukin-8 and tumour necrosis factor-alpha in induced sputum from patients with chronic obstructive pulmonary disease or asthma, Am. J. Respir. Crit. Care. Med., 1996, 153, 530–534
  • [11] Standards for the diagnosis and treatment of patients with COPD, ATS/ERS Guidelines., 2004,
  • [12] Standardised methodology of sputum induction and processing, ATS/ERS Guidelines., 2002,
  • [13] Kaplan L.A., Pesce A.J., Clinical Chemistry. Theory, analysis and correlation, 3rd Edition., 1996
  • [14] Trotter J., WinMDI 2.8 software package, 2000,
  • [15] Tkacova R., Kluchova Z., Joppa P., Petrasova D., Molcanyiova A., Systemic inflammation and systemic oxidative stress in patients with acute exacerbations of COPD, Respir. Med., 2007, 101, 1670–1676[Crossref][WoS]
  • [16] Yoshikawa T., Dent G., Ward J., Angco G., Nong G., Nomura N., et al., Impaired neutrophil chemotaxis in chronic obstructive pulmonary disease, Am. J. Respir. Crit. Care. Med., 2007, 175, 473–479[Crossref]
  • [17] Fialkow L., Wang Y., Downey G.P., Reactive oxygen and nitrogen species as signaling molecules regulating neutrophil function, Free. Radic. Biol. Med., 2007, 42, 153–164[WoS][Crossref]
  • [18] Koay M.A., Christman J.W., Segal B.H., Venkatakrishnan A., Blackwell T.R., Holland S.M., et al., Impaired pulmonary NF-κB activation in response to lipopolysaccharide in NADPH oxidase-deficient mice, Infect Immun., 2001, 69, 5991–5996[Crossref]
  • [19] Yang S., Panoskaltsis-Mortari A., Shukla M., Blazar B.R., Haddad I.Y., Exuberant inflammation in nicotinamide adenine dinucleotide phosphateoxidase- deficient mice after allogeneic marrow transplantation, J. Immunol., 2002, 168, 5840–5847
  • [20] Babior B.M., Lambeth J.D., Nauseef W., The neutrophil NADPH oxidase, Arch. Biochem. Biophys., 2002, 397, 342–344[Crossref]
  • [21] Cianchetti S., Bacci E., Ruocco L., Bartoli M.L., Ricci M., Pavia T., Dente F.L, Franco A., Vagaggini B., Paggiaro P.L., Granulocyte markers in hypertonic and isotonic saline-induced sputum of asthmatic subjects, Eur. Respir. J., 2004, 24, 1018–1024[Crossref]
  • [22] Rizoli S.B., Rotstein O.D., Parodo J., Phillips M.J., Kapus A., Hypertonic inhibition of exocytosis in neutrophils: central role for osmotic actin skeleton remodeling., Am. J. Physiol. Cell. Physiol., 2000, 279, C619–C633
  • [23] Junger W.G., Hoyt D.B., Davis R.E., Herdon-Remelius C., Namiki S., Junger H., Loomis W., Altman A., Hypertonicity regulates the function of human neutrophils by modulating chemoattractant receptor signaling and activating mitogen-activated protein kinase p38, J. Clin. Invest., 1998, 109, 2768–2779[Crossref]
  • [24] Rahman I., Oxidative stress, transcription factors and chromatin remodelling in lung inflammation, Biochem. Pharmacol., 2002, 64, 935–942[Crossref]
  • [25] MacNee W., Oxidative stress and lung inflammation in airways disease, Eur. J. Pharmacol., 2001, 429, 195–207[Crossref]
  • [26] Quint J.K., Wedzicha J.A., The neutrophil in chronic obstructive pulmonary disease, J. Allergy. Clin. Immun., 2007, 119, 1065–1071[Crossref]
  • [27] O’Donnell R., Breen D., Wilson S., Djukanovic R., Inflammatory cells in the airways in COPD, Thorax, 2006, 61, 448–454[Crossref]
  • [28] Moodley Y.P., Krishnan V., Lalloo U.G., Neutrophils in induced sputum rise from central airways, Eur. Respir. J., 2000, 15, 36–40[Crossref]
  • [29] Gaudry M., Caon A.C., Gilbert C., Lille S., Naccache P.H., Evidence for the involvement of tyrosine kinases in the locomotory responses of human neutrophils, J. Leukocyte. Biol., 1992, 51, 103–108
Document Type
Publication order reference
YADDA identifier
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.