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