Inflammatory response to sputum induction measured by exhaled markers.
BACKGROUND
Sputum induction is increasingly used to study both cellular and biochemical composition of the airways. However, there is a significant rise in the percentage of neutrophils at 8 h after inhalation with hypertonic saline.


OBJECTIVE
The aim of this study was to assess whether markers of inflammation in exhaled air and exhaled air condensate change after sputum induction in normal and asthmatic subjects.


METHODS
We measured leukotriene B(4) (LTB(4)) and a marker of oxidative stress, 8-isoprostane, (by enzyme immunoassay) in exhaled air condensate and exhaled nitric oxide (NO; by chemiluminescence analyzer) in 15 healthy subjects (8 females, mean age 35 +/- 4 years, FEV(1) 97.4% predicted) and in 8 mild asthmatic subjects (5 males, mean age 34 +/- 2 years, FEV(1) 70.5% predicted).


RESULTS
LTB(4) was significantly higher compared with baseline at 6 h but did not remain increased at 24 h after sputum induction (134.3 +/- 30.15 and 75.4 +/- 14.32 vs. 64.6 +/- 11.6 pg/ml at baseline; p < 0.02 and p > 0.05, respectively) in healthy subjects. An inverse correlation between LTB(4) and exhaled NO at 6 h after sputum induction was observed in healthy subjects (r = -0.66, p < 0.03). No increase in LTB(4) levels was observed in asthmatic patients. Baseline 8-isoprostane levels were higher in asthmatic patients than in healthy subjects (47.3 +/- 37.1 vs. 17.5 +/- 8.8 pg/ml; p < 0.01). A trend towards increased levels of 8-isoprostane could be observed at 6 and 24 h after inhalation in healthy subjects (26.2 +/- 3.7 and 26.7 +/- 3.9 pg/ml; p = 0.09 and p = 0.07, respectively). In healthy subjects, exhaled NO was significantly higher compared with baseline at 6 h and remained increased 24 h after sputum induction (7.96 +/- 3.5 vs. 5.61 +/- 1.86 ppb; p < 0.01 and p < 0.05, respectively). Exhaled NO levels were increased in asthmatic patients but did not further increase after sputum induction.


CONCLUSIONS
Sputum induction with hypertonic saline causes an inflammatory response which should be considered when using the technique to monitor airway inflammation.
Antczak
Adam
A
Department of Pneumology and Allergology, Medical University of Lodz, Kopcinskiego str. 22, PL-90-153 Lodz, Poland.
Kharitonov
Sergei A
SA
Montuschi
Paolo
P
Gorski
Pawel
P
Barnes
Peter J
PJ
D000328:Adult; D001249:Asthma / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism*; D002248:Carbon Monoxide / Q000378:metabolism; D003948:Diagnostic Techniques, Respiratory System / Q000009:adverse effects*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000378:metabolism; D045853:Exhalation; D005260:Female; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D007975:Leukotriene B4 / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D013183:Sputum / Q000378:metabolism*
D015415:Biomarkers; D007975:Leukotriene B4; C075750:8-epi-prostaglandin F2alpha; D009569:Nitric Oxide; D002248:Carbon Monoxide; D015237:Dinoprost