BACTERIAL LIPOPOLYSACCHARIDE-INDUCED SULFIDOLEUKOTRIENE RELEASE FROM PERIPHERAL-BLOOD LEUKOCYTES IN PATIENTS WITH ASTHMA AND CHRONIC OBSTRUCTIVE PULMONARY-DISEASE

Citation
M. Krausfilarska et al., BACTERIAL LIPOPOLYSACCHARIDE-INDUCED SULFIDOLEUKOTRIENE RELEASE FROM PERIPHERAL-BLOOD LEUKOCYTES IN PATIENTS WITH ASTHMA AND CHRONIC OBSTRUCTIVE PULMONARY-DISEASE, Journal of investigational allergology & clinical immunology, 8(2), 1998, pp. 94-97
Citations number
28
Categorie Soggetti
Allergy,Immunology
ISSN journal
10189068
Volume
8
Issue
2
Year of publication
1998
Pages
94 - 97
Database
ISI
SICI code
1018-9068(1998)8:2<94:BLSRFP>2.0.ZU;2-V
Abstract
Bacterial endotoxins are seen to possess strong proinflammatory activi ties. These substances may intensify inflammation in the airways of pa tients with chronic obstructive pulmonary disease (COPD) and asthma by facilitating release of various mediators from different types of cel ls. Sulfidoleukotrienes (sLT) cause bronchoconstriction, increase vasc ular permeability and stimulate mucous secretion. The aim of our study was to evaluate sLT release from peripheral blood leukocytes stimulat ed by Klebsiella pneumoniae lipopolysaccharide (LPS) and obtained from COPD and asthma patients. Nineteen subjects with mild or moderate sta ble bronchial asthma, nine patients with COPD and 10 healthy controls entered the study, Cellular allergen stimulation test (CAST)-ELISA tes t was performed using Buhlmann Laboratories AG kits io determine sLT p roduction. The differences between atopic (462.57 SD=215.89 pg/ml) and nonatopic (474.25 SD=158.02 pg/ml) asthmatics in comparison to health y controls (191.55 SD= 53.2 pg/ml) were statistically significant (p < 0.005) upon LPS stimulation at the concentration of 10 mu g/ml. At low er LPS concentration (1 mu g/ml) the difference was statistically sign ificant only between nonatopic asthmatics and healthy subjects (p <0.0 2). In the COPD group the sLT production in either LPS concentration w as higher than in the controls but the difference was not significant. We suppose that leukocytes obtained from asthmatics and COPD patients are more susceptible to LPS than these cells it-om healthy individual s. An increased sLT production upon LPS stimulation during respiratory bacterial infection may increase inflammation, bronchoconstriction an d increase nonspecific branchial hyperreactivity.