FIGURE SUMMARY
Title

Early Life Glucocorticoid Exposure Modulates Immune Function in Zebrafish (Danio rerio) Larvae

Authors
van den Bos, R., Cromwijk, S., Tschigg, K., Althuizen, J., Zethof, J., Whelan, R., Flik, G., Schaaf, M.
Source
Full text @ Front Immunol

Experimental time-line of the different experiments. dex, dexamethasone.

(A) Regression scores (mean ± SEM) of components 1 and 2 from the PCA for the different treatments (cortisol or control) and strains (AB or TL). Genes that contributed to the components are indicated in the figure. One subject was removed from the statistical analyses (TL control) as it was a consistent outlier following Grubb's outlier test. (B) Regression scores (mean ± SEM) of the only component of the PCA for the different treatments (dexamethasone or control) and strains (AB or TL). Genes that contributed to the component are indicated in the figure.

(A) Number of neutrophils and macrophages (mean ± SEM) at 4 hpa for the different treatments (cortisol or control). (B) Number of neutrophils and macrophages (mean ± SEM) at 4 hpa for the different treatments (dexamethasone or control). In both panels the picture illustrates the position of the site of the tail fin amputation in 3 dpf larvae. **p = 0.01 (Student's t-test).

(A) Per cent of surviving larvae following LPS treatment (from 0 to 0.5 h) and 0–6 hpf control treatment, cortisol treatment or dexamethasone treatment in the first exposure series (time-points: 0, 4, and 28 h). (B) Per cent of surviving larvae following LPS treatment (from 0 to 0.5 h) and 0–6 hpf control treatment, cortisol treatment and dexamethasone treatment in second exposure series (time-points: 0, 0.5, 1, 3, 6, and 24 h).

(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.

(A) Per cent of larvae following LPS treatment (from 0 to 0.5 h) in the 0–6 hpf control treatment group showing normal, swollen, or damaged tail fins (time-points: 0, 0.5, 1, 3, 6, and 24 h). (B) Per cent of larvae following LPS treatment (from 0 to 0.5 h) in the 0–6 hpf cortisol treatment group showing normal, swollen or damaged tail fins (time-points: 0, 0.5, 1, 3, 6, and 24 h). (C) Per cent of larvae following LPS treatment (from 0 to 0.5 h) in the 0–6 hpf dexamethasone treatment group showing normal, swollen, or damaged tail fins (time-points: 0, 0.5, 1, 3, 6, and 24 h).

(A) Transcript abundance (relative normalized expression; mean+SEM) of tlr44bb 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). (B) Transcript abundance (relative normalized expression; mean + SEM) of IL1β 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). (C) Transcript abundance (relative normalized expression; mean + SEM) of myd88 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). (D) Transcript abundance (relative normalized expression; mean+SEM) of IL10 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). (E) Transcript abundance (relative normalized expression; mean+SEM) of cxcr4a 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).

Acknowledgments
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