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. 2021 Apr 28;12:2460. doi: 10.1038/s41467-021-22814-9

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© The Author(s) 2021

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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Fig. 5 — Cytokine concentrations were measured in samples of ETA collected over the course of infection. Panel A places cytokine sampling points into the context of the infection. Panels B–E show levels of cytokines that have been shown to protect against P. aeruginosa infection. A single measure of cytokine abundance was taken from each ETA sample due to the high reproducibility of these assays. Reference shows the abundance of cytokines in critically ill patients from the ASPIRE-ICU study who did not develop pneumonia (mean + /− s.e.m; n = 6 patients). F LL-37 tolerance of lung isolates, as measured by the rate of cell death at a fixed dose of LL-37 (50 μg/mL). Plotted points show death rate of each genotype (mean + /− s.e.m; n = 3 isolates). Increased LL-37 tolerance was only found in all mutants, as determined by a two-tailed Dunnett’s test treating the ancestral strain as a control group. Source data are provided as a Source Data file.