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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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CS and HIV individually and additively suppress CFTR biogenesis and function. NHBE ALI cultures were infected with either R5- (HIV BaL) or X4- (HIV IIIB) tropic strain of HIV and exposed to chronic smoke exposure on days 0, 3, 6 and 9 (air as control). On day 9, total RNA was analyzed for CFTR mRNA by qRT-PCR. Another set of age and lung-matched cultures grown on snapwells were treated similarly and mounted in Ussing chambers on day 9. Cells were mounted in Ussing chambers and Cl^- efflux in response to albuterol addition was determined in the presence of amiloride as reported by us earlier⁵. HIV infection and CS individually and additively suppresses CFTR mRNA and function (panels a,b). n = 3 lungs (unless stated otherwise) *significant; S = significant from each other (p < 0.05).