IL-18 might reflect disease activity in mild and moderate asthma exacerbation.
BACKGROUND
IL-18, identified as an IFN-gamma-inducing factor, is a proinflammatory cytokine that plays an important role in TH1 cell activation. Recently, it was reported that histamine induced IL-18 and that IL-18 might act as a coinducer of TH1 and TH2 cytokines.


OBJECTIVE
The aim was to evaluate the contribution of IL-18 to asthma exacerbation.


METHODS
Serum IL-18, soluble IL-2 receptor, eosinophil cationic protein, and plasma IFN-gamma levels, as well as peak expiratory flow were measured in patients with stable asthma (n = 28), acute mild or moderate asthma (n = 23), or pulmonary sarcoidosis (n = 35) and in healthy subjects (n = 26). We compared the serum IL-18 levels between patients with acute asthma and those in remission and examined the time course in acute exacerbation after asthma therapy.


RESULTS
Significantly higher serum IL-18 levels were found in patients with acute asthma (215 +/- 33 pg/mL, mean +/- SE; P = .02) and pulmonary sarcoidosis (239 +/- 27 pg/mL, P = .008) than in control subjects (127 +/- 11 pg/mL), but the plasma IFN-gamma level was significantly elevated in only pulmonary sarcoidosis (P < .001). In pulmonary sarcoidosis the IL-18 values significantly correlated with the IFN-gamma levels (r = 0.61, P < .001), but in acute asthma they did not. The IL-18 levels during acute asthma exacerbation were significantly higher (P = .01) than on remission days. In acute asthma, circulating IL-18 levels significantly correlated with serum soluble IL-2 receptor levels (r = 0.77, P < .0001) but not with serum eosinophil cationic protein levels. The IL-18 level had a tendency to inversely correlate with peak expiratory flow. The elevated IL-18 levels in acute asthma quickly decreased on day 3 (P = .02) and day 7 (P = .002) after therapy.


CONCLUSIONS
It was suggested that IL-18 may play a potential role to activate immunologic responses and may reflect disease activity in mild and moderate asthma exacerbation.
Tanaka
H
H
Third Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Miyazaki
N
N
Oashi
K
K
Teramoto
S
S
Shiratori
M
M
Hashimoto
M
M
Ohmichi
M
M
Abe
S
S
D000208:Acute Disease; D000368:Aged; D001249:Asthma / Q000097:blood*; D001798:Blood Proteins / Q000032:analysis; D016207:Cytokines / Q000378:metabolism; D047091:Eosinophil Granule Proteins; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000097:blood; D020382:Interleukin-18 / Q000097:blood*; D008171:Lung Diseases / Q000097:blood; D008297:Male; D008875:Middle Aged; D010366:Peak Expiratory Flow Rate; D015375:Receptors, Interleukin-2 / Q000097:blood; D012260:Ribonucleases; D012507:Sarcoidosis / Q000097:blood; D012995:Solubility; D018418:Th2 Cells / Q000378:metabolism
D001798:Blood Proteins; D016207:Cytokines; D047091:Eosinophil Granule Proteins; D020382:Interleukin-18; D015375:Receptors, Interleukin-2; D007371:Interferon-gamma; D012260:Ribonucleases