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CCL18 Production is Decreased in Alveolar Macrophages from Cigarette Smokers

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Abstract

It is generally known that cigarette smoke alters the activation of alveolar macrophages (AM). CC Chemokine Ligand 18 (CCL18) is a marker of alternatively activated macrophages and is highly expressed in the lung. This study examines the influence of chronic cigarette smoking on the expression of CCL18 by AM. Bronchoalveolar lavage (BAL) and serum were obtained from ten smokers and 14 non-smokers. CCL18 protein concentrations were measured in serum and BAL fluid (BALF) as well as in supernatants from BAL-cells by enzyme-linked immunosorbent assay. In this study we show that the CCL18 production of BAL-cells from smokers was significantly decreased compared to BAL-cells from non-smokers. The BALF CCL18 protein concentration per macrophage cell count was significantly reduced in smokers. Furthermore, we show a decrease in CCL18 production from BAL-cells after stimulation with LPS. This decrease in CCL18 production was only shown in BAL-cells from non-smokers, which is probably due to chronic LPS exposure of smokers, resulting in LPS hypo-responsiveness. No statistically significant difference of CCL18 concentrations was found in BALF or serum of smokers versus non-smokers. CCL18 production by BAL-cells is down-regulated by chronic cigarette smoking and LPS contamination in cigarette smoke might be one factor involved. Thus this article gives further evidence that chronic cigarette smoking alters the phenotype of AM and that the M2 marker CCL18 is down-regulated in smokers macrophages.

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Authors and Affiliations

  1. Department of Pneumology, Medical Center, Albert-Ludwigs University, Killianstr. 5, 79106, Freiburg, Germany

    Florian Kollert, Corina Probst, Joachim Müller-Quernheim, Gernot Zissel & Antje Prasse

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  1. Florian Kollert
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  2. Corina Probst
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  3. Joachim Müller-Quernheim
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  4. Gernot Zissel
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  5. Antje Prasse
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Correspondence to Antje Prasse.

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Kollert, F., Probst, C., Müller-Quernheim, J. et al. CCL18 Production is Decreased in Alveolar Macrophages from Cigarette Smokers. Inflammation 32, 163–168 (2009). https://doi.org/10.1007/s10753-009-9115-5

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