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Biomedical subjects

F J Van Overveld

Publications and source records attributed to F J Van Overveld.

9 recordsLinked to original sources
PubMed2006

Differences in responses upon corticosteroid therapy between smoking and non-smoking patients with COPD.

Inhaled corticosteroids have a high level of topical anti-inflammatory activity. However, in patients with COPD these drugs have been reported to exert limited effects. A reduction in histone deacetylase (HDAC) activity is suggested to prevent the anti-inflammatory action of corticosteroids. Cigarette smoke is known to reduce HDAC expression. The aim of this study is to compare the outcome of corticosteroid therapy in both smoking and non-smoking COPD patients. Twenty-three smoking patients and 18 ex-smoking patients with COPD were treated with inhaled corticosteroids for a period of 2 months. Blood and induced sputum samples were collected before and after treatment. Values of FEV(1) %-predicted did not change upon the therapy, but there was a trend to improve in the ex-smokers (63.1 -> 64.8%-pred.), compared with a decrease in the smokers (63.3 -> 61.6%-pred.). The levels of the pro-inflammatory cytokine IL-8 increased in the group of smokers from 379 +/-78 to 526 +/-118 ng/ml. Although not significant, a slight decrease from 382 +/-70 to 342 +/-62 ng/ml was observed in the group of ex-smokers. The neutrophil related elastase activity showed similar effects after steroid treatment, it went up from 36.4 +/-12.0 to 113.5 +/-9.7 nmol/l in smokers, and decreased from 346.2 +/-72.1 to 131.1 +/-6.5 nmol/l in ex-smokers with COPD. These results support the evidence that inhaled corticosteroids have no anti-inflammatory effects in COPD patients, but only when these patients are still smoking. Smoking cessation seems the best therapy for COPD patients.

Adrenal Cortex Hormones↗
PubMed2006

Influence of N-acetylcysteine on ICAM-1 expression and IL-8 release from endothelial and epithelial cells.

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation. The initial step in the inflammatory process is overexpression of adhesion molecules, which leads to excessive transmigration of neutrophils. One of these adhesion molecules is ICAM-1 which is elevated in COPD patients. In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines. The methodology used consisted of immunochemistry for the assessment of surface ICAM-1 and ELISA method for that of soluble ICAM-1 and IL-8. NAC inhibited the TNF-alpha/IL-1 beta-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner. The most effective concentrations were 30 mM and 20 mM (99 and 90% inhibition respectively, P<0.01). We conclude that NAC is an effective inhibitor of TNF-alpha/IL-1 beta- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells. This fact highlights the anti-inflammatory potential of NAC in COPD.

Acetylcysteine↗
PubMed1992

Synergism between interleukin-1 beta and interferon-gamma, an inducer of nitric oxide synthase, in rat lung fibroblasts.

An L-arginine-dependent pathway, by which L-arginine is metabolised to citrulline and nitrogen oxides, has been recently identified in some cell types. In cultured rat lung fibroblasts the presence of L-arginine was necessary for the production of nitrite to be induced by rat recombinant interferon-gamma and synergistically enhanced by lipopolysaccharide and interleukin-1 beta. Lipopolysaccharide and interleukin-1 beta did not induce nitrite biosynthesis by themselves. Biosynthesis was apparently dependent on tetrahydrobiopterin, since it could be blocked by diaminohydroxypyrimidine, an inhibitor of tetrahydrobiopterin synthesis. Dexamethasone blocked nitrite production by a receptor-mediated mechanism. These data indicate that rat lung fibroblasts express an L-arginine-dependent nitric oxide synthase which can be induced by some mediators of inflammation.

Amino Acid Oxidoreductases↗
PubMed1992

Soybean trypsin inhibitor and beta-amylase induce alveolar macrophages to release nitrogen oxides.

Rat alveolar macrophages incubated with soybean trypsin inhibitor and beta-amylase produced nitrite in a dose- and time-dependent manner. This production depends on the presence of L-arginine (L-arg) in the culture medium. The precursor of this nitrite was demonstrated as being nitric oxide by bleaching ferredoxin at 410 nm when added to the culture medium. NG-Monomethyl-L-arginine and the tetrahydrobiopterin biosynthesis inhibitor 2,4-diamino-6-hydroxypyrimidine inhibited the release of nitrite in a dose-dependent manner. Dexamethasone was able to modulate this release. These data indicate that alveolar macrophages are capable of secreting L-arg-derived nitrogen oxides when stimulated with certain alimentary proteins.

Animals↗
PubMed1991

L-arginine-dependent production of nitrogen oxides by rat pulmonary macrophages.

Rat alveolar and pleural macrophages incubated with lipopolysaccharide, opsonized zymosan or recombinant interferon-gamma, but not with recombinant tumor necrosis factor-alpha, produced nitrite dose and time dependently. This production depends on the presence and amount of L-arginine in the culture medium. The precursor of the nitrite was demonstrated as being nitric oxide, by bleaching of ferredoxin at 410 nm when added to the culture medium. Addition of NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthesis, and cycloheximide, a protein synthesis inhibitor, to the medium resulted in a decrease of nitrite production. Glucocorticoids were able to block the induction of nitrite production in alveolar macrophages. These data indicate that pulmonary macrophages are capable of secreting L-arginine-derived nitrogen oxides.

Animals↗
PubMed1989

Mast cell heterogeneity in human lung tissue.

1. In this study mast cells were found to comprise 2.1% of total cells recovered by enzymatic digestion of human lung tissue. 2. This mast cell population consisted of 79% formalin-sensitive, Alcian Blue-positive mast cells and 21% formalin-insensitive, Alcian Blue-positive mast cells. 3. By the use of centrifugal elutriation and subsequent Percoll gradient centrifugation, separate mixed cell populations could be obtained in which the mast cell constituents were either of the formalin-sensitive or -insensitive type. 4. Cell suspensions in which formalin-sensitive cells comprised 97% of mast cells contained approximately 1.34 pg of histamine per mast cell, whereas in preparations in which mast cells were 84% formalin-resistant the histamine content was approximately 4.17 pg of histamine per mast cell. 5. The histamine release upon anti-immunoglobulin E challenge of formalin-sensitive mast cells was greater than the release by formalin-insensitive mast cells. 6. After challenge with opsonized zymosan, only formalin-sensitive mast cells were able to release histamine. 7. Leukotriene C4 release was observed when formalin-sensitive mast cells were challenged with anti-immunoglobulin E. Formalin-insensitive mast cells showed no release of leukotriene C4. 8. Prostaglandin D2 release was observed when formalin-insensitive mast cells were challenged with anti-immunoglobulin E. Formalin-sensitive mast cells showed no release of prostaglandin D2.

Alcian Blue↗
PubMed1989

Patients with chronic bronchitis differ in their mast cell subtypes as compared with normal subjects.

Mast cells were isolated by enzymatic digestion from lung tissue obtained from patients with chronic obstructive lung disease and from normal subjects. Two mast cell subtypes could be demonstrated in human lung tissue. Mast cell subtypes were differentiated in formalin-sensitive and formalin-insensitive mast cells. It appeared that compared with normal individuals, patients suffering from chronic bronchitis had increased numbers of mast cells of the formalin-sensitive type, whereas patients with emphysema had reduced numbers, but the same ratio, of both mast cell subtypes.

Aged↗