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Department
of Thoracic Medicine, National Heart & Lung Institute, Imperial College
School of Medicine, Dovehouse Street, London SW3 6LY, UK
Correspondence to: Dr J A Nightingale.
Received 30 December 1997; Returned to authors 9 March 1998; Revised version received 31 March 1998; Accepted for publication 31 March 1998
BACKGROUND
Inhalation
of lipopolysaccharide (LPS) causes an inflammatory response in the
lungs. To explore this response, inflammatory indices were measured in
induced sputum from atopic asthmatic patients and compared with atopic
and non-atopic subjects after inhalation of LPS.
METHODSThe
effects of inhaled LPS (60 µg) or placebo (0.9% saline) were
examined in a randomised, double blind, crossover trial in 11 non-atopic normal subjects, seven atopic, non-asthmatic
individuals, and eight atopic, asthmatic patients. Sputum was
induced by inhalation of 3.5% saline before the test inhalation
and again at six hours and 24 hours. Spirometry (forced expiratory
volume in one second (FEV1), forced vital capacity
(FVC)), heart rate, blood pressure, and temperature were recorded
before challenge and at intervals until eight hours, and at 24 hours
after challenge.
RESULTSThere
was no change in cardiovascular parameters or spirometry with either
exposure in any group. In the asthmatic patients only, inhalation
of LPS caused a rise in temperature, with a peak of 0.6°C at seven
hours, which was significantly higher than following placebo
inhalation (p<0.05). In normal subjects, LPS caused a significant rise
in absolute neutrophil counts at 24 hours compared with placebo (median
1.1 × 106 cells/ml after LPS; median 0.2 × 106 cells/ml after placebo, p<0.01), but no change in
differential counts. In asthmatic patients, LPS caused a significant
rise in differential neutrophil counts at six hours compared with
placebo (median 88% after LPS; median 56% after placebo, p<0.05),
but no change in absolute cell counts at any time point. There was no
change in neutrophil counts in the atopic subjects. There was a
significant rise in sputum interleukin 8 (IL-8) concentrations in
normal subjects at six hours compared with placebo (mean placebo 1.1 ng/ml; LPS 3.0 ng/ml, p<0.05) and in asthmatics at 24 hours (mean
placebo 2.0 ng/ml, LPS 6.9 ng/ml, p<0.05). There were no changes in
sputum concentrations of tumour necrosis factor 
or granulocyte
macrophage colony stimulating factor at any time.
CONCLUSIONSInhalation
of LPS causes a neutrophilic inflammation with increases in IL-8 in
both normal and asthmatic subjects.
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