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. 2018 May 22;8:7984. doi: 10.1038/s41598-018-26095-z

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Effect of CS exposure on CCR5 Cell surface receptor quantified by Single Cell Imaging flow cytometry. NHBE ALI cultures were exposed to CS. At the end of smoking, cells were immuno-stained with surface markers anti-human CCR5 labeled with APC. Percent Gated CCR5+ or APC+ cells for air NHBE (8.58 ± 2.85%) and smoke NHBE (20.25 ± 4.5%, P = 0.03) are represented (panel a). MFI of APC from in total population of cell images acquired (10,000 per sample) for air NHBE cells (818.74 ± 274.02) and smoked NHBE cells (1494.16 ± 447.95) are represented (panel b). Representative overlay histogram of intensity of APC for isotype control (yellow), air (blue) and smoke (green) (panel c). A representative single cell image for each sample is shown (panel d). Experiments were carried out from at least 3 different lungs. *Significant (p < 0.05).