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. 2019 Jun 11;9:8514. doi: 10.1038/s41598-019-44955-0

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© The Author(s) 2019

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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Pulmonary cytosolic IκB degradation in response to systemic LPS is not different between neonatal male and female mice. Representative Western blots of pulmonary cytosolic extracts showing (A,B) IκBα and IκBβ, (C) p105 and (D) IKKβ in neonatal (P0) male and female mice following exposure to systemic LPS (5 mg/kg IP, 1–5 hours). Calnexin as loading control. Densitometric analysis of (E) IκBα, (F) IκBβ, (G) p105 and (F) IKKβ in pulmonary cytosolic extracts form neonatal male and female mice following exposure to systemic LPS (5 mg/kg IP, 1–5 hours). All values first normalized to loading control, then to unexposed, sex-specific control. Values shown as means ± SEM from 6 individual animals per sex per time point. *p < 0; 0.05 vs. control.