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. 2017 Aug 16;7:8304. doi: 10.1038/s41598-017-08588-5

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© The Author(s) 2017

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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A model of the possible involvement of damaged SP-A in CS-induced innate immune dysfunction. (A) The lung is continuously exposed to airborne pathogens. SP-A protects the lung by inhibiting bacterial growth and inducing macrophage phagocytic activity¹². (B) SP-A damage by CS attenuates its ability to inhibit bacterial growth and induce macrophage phagocytosis. The structural and functional disruption of SP-A may thus contribute to CS-induced innate immune dysfunction.