SUMMARYThe inflammatory process in chronic obstructive pulmonary disease (COPD) is active mainly in the airways, but little is known about the properties of the inflammatory cells in this compartment. We have studied leucocytes in induced sputum of COPD patients compared to controls in order to uncover what types of macrophages might be involved in the disease. Sputum induction was performed by inhalation of nebulized sodium chloride solution. Leucocytes were isolated and stained with specific monoclonal antibodies for analysis in flow cytometry. Flow cytometry analysis revealed that a major portion of CD14 + macrophages in COPD has lower forward scatter, i.e. they are small macrophages. While in control donors these small macrophages accounted for 6·9% of all macrophages, the percentage of these cells in COPD was 45·7%. CD14 and HLA-DR expression was high on these small sputum macrophages while the large sputum macrophages expressed only low levels of these surface molecules, both in control donors and COPD patients. Small sputum macrophages of both control donors and COPD patients showed higher levels of constitutive tumour necrosis factor (TNF) compared to the large macrophages. TNF was inducible by lipopolysaccharide (LPS) preferentially in the small sputum macrophages in the control donors but there was no further induction in COPD patients. These data show that the small sputum macrophages are a major macrophage population in COPD and that these cells exhibit features of highly active inflammatory cells and may therefore be instrumental in airway inflammation in COPD.
A Ac ct ti iv va at ti io on n o of f t th he e t tr ra an ns sc cr ri ip pt ti io on n f fa ac ct to or r N NF F--κB B i in n h hu um ma an n t tr ra ac ch he eo ob br ro on nc ch hi ia al l e ep pi it th he el li ia al l c ce el ll ls s b by y i in nf fl la am mm ma at to or ry y s st ti im mu ul li i In this study, we asked whether the multiunit transcription factor, nuclear factor (NF)-κB, which regulates the expression of genes involved in defence and immune processes, is activated in airway epithelial cells following stimulation with inflammatory mediators and hydrogen peroxide. In addition, we studied whether this would be followed by upregulation of the NF-κB target gene product granulocytemacrophage colony-stimulating factor (GM-CSF). Activation of NF-κB in the SV40 transformed human tracheobronchial epithelial cell line 1HAEo-was measured by electrophoretic mobility shift assays. GM-CSF concentrations in cell culture supernatants were determined by enzyme-linked immunosorbent assays. These results suggest that NF-κB may represent an important transcription factor, controlling the expression of cytokine genes in airway epithelial cells. NF-κB was rapidly activated by exposure of cells to interleukin-1β (IL-1β), phorbol myristate acetate (PMA), and tumour necrosis factor-α (TNF). Exposure to
Since asymptomatic, nonspecific airway hyperresponsiveness (BHR) may be due to an enhanced local inflammatory response, we studied molecular markers of inflammation in induced sputum from subjects with asymptomatic BHR (n = 14) compared with control subjects (n = 13) and patients with chronic obstructive pulmonary disease (COPD) (n = 10). Pulmonary lung function parameters were measured by spirometry and body plethysmography. Hyperresponsiveness was defined based on histamine challenge. Induced sputum samples were collected and the solid phase was isolated and analyzed for leukocyte numbers and differential and for cytokines (ELISA). IL-8 was 2.4-fold increased (p = 0.036) in the sputum of subjects with asymptomatic BHR (24.8 +/- 22.0 ng/mL; +/- SD) and 11.2-fold enhanced in patients with COPD (117.8 +/- 106.3 ng/mL) as compared with control subjects (10.5 +/- 7.7 ng/mL). In control subjects, no IL-5 was measured, however, sputum of those with asymptomatic BHR contained IL-5 at 0.044 +/- 0.090 ng/mL fluid and COPD patients at 1.00 +/- 2.01 ng/mL. GM-CSF could not be detected in sputum samples of any subjects investigated. Number of total leukocytes was higher in those with asymptomatic BHR and COPD (with BHR: 9.4 +/- 10.8 x 10(5); COPD: 83.5 +/- 182.5 x 10(5)) compared with persons without BHR (2.9 +/- 3.4 x 10(5)). PMN were increased in patients with asymptomatic BHR (4.1 +/- 5.3 x 10(5)) (38.8 +/- 24.7%) and COPD (32.9 +/- 71.0 x 10(5)) (75.4 +/- 18.6%) compared with controls (0.7 +/- 0.9 x 10(5)) (25.8 +/- 25.7%). In contrast to PMN counts in those with asymptomatic BHR (0.06 +/- 0.11 x 10(5)) (1.5 +/- 3.7%), eosinophil counts were only slightly increased compared with control subjects (0.01 +/- 0.02 x 10(5)) (0.6 +/- 0.9%). This study supports the hypothesis that BHR in asymptomatic people is associated with airway inflammation that may predispose to development of chronic diseases such as COPD.
The seed coat of almond (Prunus amygdalus Batsch) contains up to 30% procyanidins with different degrees of polymerisation and, in addition, fatty oils, lignin, polysaccharides and cutin. Monomer units of dimers to tetracosamers are (-)-epicatechin and (+)-catechin. Prodelphinidins could not be detected. The dimers B-1, B-3, B-4, trimers and oligomers are soluble in acetone/water. The bulk material is large polymer, that is only soluble, by thiolysis, in thioglycolic acid. The large polymer procyanidins are crucial to the structure and attributes of the seed coat.
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