Source: Annual Congress 2011 - Bronchoalveolar lavage and biomarkers in diffuse parenchymal lung disease
Disease area: Interstitial lung diseases

Abstract

BACKGROUND. Cigarette smoke is recognized as a cause of lung tumors, due to its carcinogenic potential. Less is known about suppressed local immune surveillance.
METHODS. Alveolar lymphocytes (AL) were obtained by bronchoalveolar lavage (BAL) in pulmonary sarcoidosis (PS, n=36), idiopathic pulmonary fibrosis (IPF, n=21) and control subjects (n=13), subdivided according to smoking status. Cytokines suspected for potential impact on antitumor immunity (TNFα, IFNγ and TGFβ) were tested by ELISA in BAL supernatants. AL were phenotyped for major subsets and cytokine receptors. AL apoptosis was examined with TUNEL and cell cycle analysis.
RESULTS. AL apoptosis rate was reduced in PS (0.7±0.2%, p<0.05) and increased in IPF (2.3±1.0%, p<0.02) nonsmokers, as compared to controls (1.1±0.3). Cigarette smoking in all groups resulted in significant increase of AL apoptosis rate (e.g. 11±7.5% in IPF smokers, p<0.05 as compared to nonsmokers). IFNγ levels were lower in all smoking subgroups than in respective nonsmokers. No changes were found in TGFβ and TNFα levels, but AL expression of TGF (CD105) and TNF (CD120a) receptors was higher in smoker subgroups (significant for CD105 in IPF and CD120a in PS).
CONCLUSIONS. The decreased immune surveillance in smokers lower airways include higher AL apoptosis rate and increased AL susceptibility to TGFβ and proapoptotic stimuli. Our findings suggest relative Th2 prevalence in smoker subgroups. It may be responsible for severe course of IPF, blunted PS symptoms and, in general, increased risk of local carcinogenesis.

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P. Kopinski, A. Dyczek, G. Przybylski, B. Balicka-Slusarczyk, A. Jarzemska, T. Wandtke, E. Pólgesek, M. Igielska (Bydgoszcz, Kraków, Poland). Mechanisms of impaired immune surveillance in lower airways of smokers. Data from bronchoalveolar lavage (BAL) harvested in selected interstitial lung diseases (ILDs) and control group. Eur Respir J 2011; 38: Suppl. 55, 4765

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