Abstract

Background:Inflammatory cytokines and chemokines have been reported to play important roles in thepathogenesis of bronchial asthma. However, no criteria for the classification of `smoker\u27 and `atopic\u27 in bronchialasthma have been defined. In this study, we compared the levels of several cytokines found in thebronchoalveolar lavage( BAL) fluid of patients classified as having bronchial asthma.Methods:Cell subpopulations in BAL fluid were counted. BAL fluid levels of interleukin( IL)-4, -5, -13,-17, and -33 and RANTES (regulated on activation, normal T cell expressed and secreted were measuredusing a bead suspension array in 36 asthma patients (13 males, 23 females;mean age, 39.5±92.8 years)who were non-smokers, 18 asthma patients( 11 males, 7 females;mean age, 30.7±2.7 years) who were exor current smokers( Brinkman index( BI):1&#8722;399), and 10 asthma patients( 9 males, 1 female;mean age,50.2±5.5 years) who were current heavy smokers( BI:&#8805; 400). Relationships were assessed by Spearman\u27srank correlation analysis.Results:The number of lymphocytes in BAL cell subpopulations of non-smokers( 25±7×103/ml) weresignificantly (p<0.05) higher than those of heavy smokers (12±3×103 /ml). The number of neutrophilswas significantly( p<0.05) higher in heavy smokers( 18±9×103/ml) than in non-smokers( 4±2×103/ml).Levels of IL-33 and RANTES were significantly (P<0.05) higher in non-smokers (26.1±7.3 pg/ml and42.8±10.3 pg/ml, respectively) than in heavy smokers (13.7±4.5 pg/ml and 27.4±5.4 pg/ml, respectively).In addition, the levels of IL-33 and RANTES in non-smokers were significantly( P<0.05) higher in atopicasthma patients (33.0±9.8 pg/ml and 47.8±14.0 pg/ml, respectively) than in non-atopic asthma patients(9.1±3.8 pg/ml and 29.5±7.8 pg/ml, respectively). A good correlation was noted between RANTES andlymphocytes (R=0.365, P<0.05) or IL-33 (R=0.561, P<0.05) in atopic asthma patients who were nonsmokers.Conclusions:Differences in the cell types of BAL fluid, as well as in the levels of IL-33 and RANTES inasthma patients with or without smoking, might reflect pathogenesis

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