Liheng Cai1†, Brian Button2†, Camille Ehre2, David B. Hill2, Mehmet Kesimer2, Richard C. Boucher2, Michael Rubinstein1, 3, *
1Curriculum in Applied Sciences and Engineering, University of North Carolina, Chapel Hill, NC 27599-3280, USA.
2Cystic Fibrosis Research and Treatment Center, University of North Carolina, Chapel Hill, NC 27599-7248, USA.
3Department of Chemistry, University of North Carolina, Chapel Hill, NC 27599-3290, USA.
†The first two authors (Cai and Button) contributed equally to this work.
The human airway surface layer (ASL) of human lungs consists of two parts: 1) an outer mucus layer in contact with air, which seizes inhaled toxicants and thus protects lungs from infection, and 2) an inner periciliary layer (PCL) that reaches from the epithelial cell surface to the top of the cilia. Traditionally it was thought that the space between cilia in the PCL is filled by a low viscosity liquid. However, our experiments indicate that probe objects smaller than the cilia spacing (~200 nm) cannot penetrate into the PCL as long as their size is larger than ~45 nm. Probe molecules with size smaller than ~45 nm penetrate into PCL, and their penetration depth increases with the decreasing of molecular size. However, only very small probe molecules with size on the order of 1 nm can reach the epithelial cell surface. Our findings suggest that, besides the mucus layer, the PCL serves as a further protective layer in preventing external objects approaching epithelial cell surface.
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