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. 2020 Apr 29;11:727. doi: 10.3389/fimmu.2020.00727

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Copyright © 2020 van den Bos, Cromwijk, Tschigg, Althuizen, Zethof, Whelan, Flik and Schaaf.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(A) Transcript abundance (relative normalized expression; mean+SEM) of cldn5a following LPS treatment (from 0 to 0.5 h) and 0–6 hpf control treatment, cortisol treatment or dexamethasone treatment (n = 4 samples per time-point). Groups with the same capitals do not significantly differ from one another (Tukey HSD following a significant treatment effect for this time-point). Note: control-treated subjects showed no significant change over time: F_{(3, 12)} = 2.009, ns. (B) Transcript abundance (relative normalized expression; mean + SEM) of cldn2 following LPS treatment (from 0 to 0.5 h) and 0–6 hpf control treatment, cortisol treatment or dexamethasone treatment (n = 4 samples per time-point). Note: control-treated subjects showed an increased expression at 3 h: F_{(3, 12)} = 13.253, p < 0.001; Tukey HSD. (C) Transcript abundance (relative normalized expression; mean + SEM) of oclnb following LPS treatment (from 0 to 0.5 h) and 0–6 hpf control treatment, cortisol treatment or dexamethasone treatment (n = 4 samples per time-point). Groups with the same capitals do not significantly differ from one another (Tukey HSD following a significant treatment effect for this time-point). Note: control-treated subjects showed no significant change over time: F_{(3, 12)} = 0.562, ns.