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1 Department of Laboratory Medicine and Respiratory Medicine, School of Medicine, Tokyo University, Bunkyo-ku, Tokyo 113; and 2 World Health Organization Collaborating Centre, Tokyo Medical College, Shinjuku-ku; and 3 Department of Diagnostic Radiology, School of Medicine, Keio University, Tokyo 160, Japan
To study the
inflammatory responses of small-airway epithelium in smokers, we
harvested enough living epithelial cells (1.97 × 106 ± 0.74 × 106) with a new ultrathin fiberscope from
the very peripheral airways of 22 current smokers and 17 subjects who
never smoked after informed consent was obtained. The cells were
keratin positive and composed mainly of nonciliated cells. The
expression levels of inflammatory markers [interleukin (IL)-8 and
intercellular adhesion molecule (ICAM)-1] were evaluated with
RT-PCR. The magnitude of the mRNA levels corrected by 
-actin
transcripts of IL-8 and ICAM-1 was significantly higher in the smokers
than in the nonsmokers (P < 0.001). Furthermore, among
current smokers, IL-8 mRNA levels correlated positively with the extent
of smoking history [in pack · years (packs/day × no. of years of smoking); r = 0.754, P < 0.001]. Spontaneously released IL-8 and soluble ICAM-1 levels (n = 12) from cultured epithelial cells were elevated in
subjects with a smoking history than in those without it (IL-8, 1,580 ± 29.6 vs. 354 ± 39.4 pg · 106
cells
1 · 24 h1;
P < 0.001; soluble ICAM-1, 356.0 ± 45.9 vs. 112.9 ± 12.9 pg · 106
cells1 · 24 h1;
P < 0.01 by Student's t-test ). In contrast, the
epithelial cells from the main bronchi did not show such differences
between smokers and nonsmokers. Our study highlighted a close link
between smoking and the expression of inflammatory mediators such as
IL-8 and ICAM-1 in small airways. Our results also suggested that this new ultrathin bronchofiberscope promised a good approach for the evaluation of cellular changes in the small airways.
smoking; interleukin-8; intercellular adhesion molecule-1; peripheral airways
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