Correlation between airway hyperresponsiveness and airway inflammation in a young adult population: eosinophil, ECP, and cytokine levels in induced sputum.
BACKGROUND
Eosinophil counts and eosinophil cationic protein (ECP) levels in the airway are elevated in asthmatic patients. However, few studies have examined the correlation between various cytokines in the sputum and airway hyperresponsiveness (AHR) in young adults with or without asthma.


OBJECTIVE
We examined the correlation between AHR and eosinophil counts or ECP, and levels of several cytokines in the sputum.


METHODS
We studied 120 nonsmoker students (group 1: intermittent mild asthmatic patients; group 2: subjects with history of childhood asthma; group 3: subjects sensitized by Dermatophagoides farinae with atopic disease; group 4: normal subjects sensitized by D. farinae; group 5: subjects with cedar pollinosis; and group 6: normal subjects). In each subject, AHR and lung function tests were measured, together with eosinophil count, ECP, granulocyte-macrophage colony-stimulating factor, TNF-alpha, IL-5, and interleukin-1beta in induced sputum.


RESULTS
AHR in groups 1 and group 2 were high, in groups 5 and 6 low, and in groups 3 and 4 lower than in groups 1 and 2 but higher than groups 5 and 6. Percentages of eosinophils, ECP, and TNF-alpha in induced sputum in groups 1 and 2 were high, those in groups 5 and 6 were below detection limits, and those in groups 3 and 4 were lower than the percentages in groups 1 and 2. Granulocyte-macrophage colony-stimulating factor in the sputum was elevated only in group 1. The correlations between AHR and sputum eosinophil count, ECP, and TNF-alpha were significant, with the strongest correlation with TNF-alpha.


CONCLUSIONS
Our results suggest that TNF-alpha levels in the sputum play an important role in determining the severity of AHR in young individuals. Further once AHR develops, it does not disappear, and the severity of airway inflammation influences the extent of AHR.
Obase
Y
Y
The Second Department of Internal Medicine, Nagasaki University School of Medicine, Japan. obadann-ngs@umin.u-tokyo.ac.jp
Shimoda
T
T
Mitsuta
K
K
Matsuo
N
N
Matsuse
H
H
Kohno
S
S
D000328:Adult; D000818:Animals; D039741:Antigens, Dermatophagoides; D001249:Asthma / Q000276:immunology*; D001798:Blood Proteins / Q000378:metabolism*; D016535:Bronchial Hyperreactivity / Q000175:diagnosis* / Q000276:immunology; D016085:Bronchoconstrictor Agents; D016207:Cytokines / Q000096:biosynthesis*; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D006023:Glycoproteins / Q000276:immunology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000096:biosynthesis; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D008297:Male; D016210:Methacholine Chloride; D011657:Pulmonary Eosinophilia / Q000097:blood / Q000276:immunology*; D011852:Radioallergosorbent Test; D012129:Respiratory Function Tests; D012260:Ribonucleases; D013183:Sputum / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D039741:Antigens, Dermatophagoides; D001798:Blood Proteins; D016085:Bronchoconstrictor Agents; D016207:Cytokines; D047091:Eosinophil Granule Proteins; D006023:Glycoproteins; D014409:Tumor Necrosis Factor-alpha; D016210:Methacholine Chloride; D007073:Immunoglobulin E; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D012260:Ribonucleases