吸烟引起哮喘支气管粘膜免疫状态改变

2007/06/27

    吸烟可导致哮喘患者对糖皮质激素反应低下,影响粘膜内树突细胞功能及数量。本文通过气道活检及免疫染色观察了吸烟对哮喘患者气道内成熟树突细胞、朗罕细胞及B淋巴细胞数量,观察了I型及II型辅助T淋巴细胞功能变化。研究结果显示,吸烟哮喘患者树突细胞及B细胞数量较非吸烟哮喘及对照人群明显减少,吸烟哮喘患者伽马干扰素表达趋于降低。研究结果提示吸烟吸烟哮喘患者大气道树突细胞及B细胞数量减少可能是激素抵抗及易发感染的原因。
 
(刘颖格 西安第四军医大学西京医院呼吸内科 710032 摘译)
       (Critical Care Medicine, 2007;175:919-925)
 
 
Cigarette Smoking Alters Bronchial Mucosal Immunity in Asthma
Maria Tsoumakidou1, William Elston1, Jie Zhu1, Zhuo Wang, Elizabeth Gamble, Nikos M. Siafakas, Neil C. Barnes and Peter K. Jeffery
 
ABSTRACT
 
Rationale: Cigarette smoking worsens asthma and is associated with reduced response to corticosteroid therapy. As cigarette smoke is known to have immunomodulatory effects, we hypothesized that one mechanism by which smoking mediates its adverse effect is by reduction of the numbers of bronchial mucosal dendritic cells (DCs), which control B-cell growth and T-cell responses.
 
Objectives: We set out to sample the bronchial mucosa in smoking and never-smoking patients with asthma and to count DCs, B cells, and cells expressing genes for two key T-lymphocyte regulatory cytokines.
 
Methods: Twenty-one never-smoker patients with asthma (6 steroid naive), 24 smoker patients with asthma (9 steroid naive), and 10 healthy never-smokers (control subjects) were recruited and their endobronchial biopsy samples were immunostained for detection of mature DCs (CD83+), Langerhans cells (CD1a+), B lymphocytes (CD20+), and helper T-cell type 1 (IFN-) and helper T-cell type 2 (IL-4) cytokine–expressing cells.
 
Measurements and Main Results: The number (per square millimeter) of CD83+ mature DCs was significantly lower in smoker patients with asthma (median [range]: 37 [0,131]) in comparison with never-smoker steroid-naive and steroid-treated patients with asthma (76 [24, 464]; p=0.006) or control subjects (85 [40,294]; p = 0.004). Moreover, B cells were fewer in smoker (26 [4, 234]) versus never-smoker steroid-naive and steroid-treated patients with asthma (45 [10, 447]; p=0.01) and in smoker steroid-naive patients with asthma (23 [4,111]) versus control subjects (34 [10, 130]; p=0.05). The number of cells expressing IFN- showed a trend toward fewer in smoker (70 [6,24]) versus never-smoker steroid-naive patients with asthma (144 [44,323]; p=0.10).
 
Conclusions: There are important and statistically significant differences in the number of CD83+ mature DCs and B cells in the large airways of smokers with asthma. We speculate that their reductions may render patients with asthma less responsive to corticosteroids and more susceptible to infection.


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