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. 2018 Jun 5;8:8652. doi: 10.1038/s41598-018-26984-3

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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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Increased pulmonary GM-CSF after acute airway inflammation and M. tuberculosis infection in vivo. WT mice were challenged intranasally with saline or LPS (1 µg/mouse) and GM-CSF levels in lung (A) and bronchoalveolar lavage (BAL) fluid (B) were measured after 24 h by ELISA. Pulmonary concentration of GM-CSF protein was measured 1 and 3 months (C) after in vivo M. tuberculosis infection (1000 ± 200 CFU/mouse i.n.) in WT mice, of after 1 month in WT and TNFα^−/− mice (D). Data are representative of two independent experiments and are expressed as mean ± SEM (n = 5–8 mice per group). The expression of GM-CSF receptor β subunits genes Csf2rb1 (E) and of Csfrb2 (F) in the lungs 4 weeks post-M. tuberculosis infection in WT and in TNFα^−/− mice was analyzed by microarray⁵⁰. Each group of infected mice has been statistically compared to the uninfected mice of the same phenotype. ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05.