Local Immune Components in Chronic Obstructive Pulmonary Disease

Costabel, Ulrich; Maier, K.L; Teschler, Helmut; Wang, Y.M.

doi:10.1159/000196097

Cited by 35 publications

(20 citation statements)

References 2 publications

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“…The discordance of these results with those showing an increase in numbers of neutrophils and markers of neutrophil activation in bronchoalveolar lavage [10,11,13,14,25], induced sputum [26±28] and airway epithelium [29] remains to be explained.…”

Section: Discussionmentioning

confidence: 85%

Subepithelial immunopathology of the large airways in smokers with and without chronic obstructive pulmonary disease

2000

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Previous work has shown an increase in CD8+ T-cells, neutrophils and eosinophils in small airway subepithelium in smokers. The authors have now investigated whether similar changes occur in the large airways.Immunohistochemistry on frozen sections of bronchial biopsies were obtained at bronchoscopy in 11 nonsmokers, eight asymptomatic smokers and 11 smokers with chronic bronchitis and chronic obstructive pulmonary disease (COPD).There was an increase in the number of CD8+ cells infiltrating the bronchial subepithelium in the COPD group compared to the asymptomatic smokers (305 (109± 400) versus 92 (41±550) cells . mm -2 , p=0.030). There was a negative correlation between the number of CD8+ cells and the forced expiratory volume in one second (FEV1) %predicted (p=0.005, r=-0.62), and a positive correlation between the number of CD8+ cells and the number of pack years smoked (p=0.017, r=0.42). There was a negative correlation between the activated/total eosinophils ratio and the FEV1 % pred (p=0.017, r=-0.51). There was a negative correlation between pack years smoked and the number of neutrophils (p=0.022, r=-0.36).Smokers who develop chronic obstructive pulmonary disease have increased numbers of CD8+ T-cells in large airways when compared to asymptomatic smokers. Airway obstruction was associated with an increase in the proportion of eosinophils that were activated. Eur Respir J 2000; 15: 512±516.

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Section: Discussionmentioning

confidence: 85%

Subepithelial immunopathology of the large airways in smokers with and without chronic obstructive pulmonary disease

2000

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“…There is good evidence for limited protein oxidation during inflammatory reactions ; for example, broncheoalveolar fluids have elevated methionine sulphoxide\methionine ratios under conditions in which leucocyte activation is apparent [221]. Furthermore, oxidized proteins (and DNA) form inside the leucocytes during their triggering, as judged by protein carbonyls [222] and tyrosine modification [223], although it is not clear whether this affects protein function directly.…”

Section: Protein Oxidation In Host Defence and Tissue Catabolismmentioning

confidence: 99%

Biochemistry and pathology of radical-mediated protein oxidation

Dean

Stocker

et al. 1997

Biochemical Journal

1,548

982

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Radical-mediated damage to proteins may be initiated by electron leakage, metal-ion-dependent reactions and autoxidation of lipids and sugars. The consequent protein oxidation is O2-dependent, and involves several propagating radicals, notably alkoxyl radicals. Its products include several categories of reactive species, and a range of stable products whose chemistry is currently being elucidated. Among the reactive products, protein hydroperoxides can generate further radical fluxes on reaction with transition-metal ions; protein-bound reductants (notably dopa) can reduce transition-metal ions and thereby facilitate their reaction with hydroperoxides; and aldehydes may participate in Schiff-base formation and other reactions. Cells can detoxify some of the reactive species, e.g. by reducing protein hydroperoxides to unreactive hydroxides. Oxidized proteins are often functionally inactive and their unfolding is associated with enhanced susceptibility to proteinases. Thus cells can generally remove oxidized proteins by proteolysis. However, certain oxidized proteins are poorly handled by cells, and together with possible alterations in the rate of production of oxidized proteins, this may contribute to the observed accumulation and damaging actions of oxidized proteins during aging and in pathologies such as diabetes, atherosclerosis and neurodegenerative diseases. Protein oxidation may also sometimes play controlling roles in cellular remodelling and cell growth. Proteins are also key targets in defensive cytolysis and in inflammatory self-damage. The possibility of selective protection against protein oxidation (antioxidation) is raised.

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“…1 For many years, the main focus of interest has been neutrophils and macrophages, but more recent pathologic and bronchoalveolar lavage (BAL) studies have suggested an important role of CD8 1 T cells in the development of COPD. [2][3][4][5] CD4 1 T lymphocytes are subclassified into T H 1 and T H 2 cells. T H 1 cells produce IFN-g, IL-2, and TNF in the absence of IL-4, IL-5, IL-9, and IL-13.…”

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confidence: 99%