What question did this study set out to answer?

To determine how elevated cortisol levels during early embryonic development alter immune function, leukocyte recruitment, and sepsis survival in zebrafish larvae.

April 29, 2020Frontiers in ImmunologyOpen Access

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

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Authors

RBRuud van den Bos SCSuzanne Cromwijk KTKatharina Tschigg

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Overview

Experimental study demonstrates enhanced sepsis survival and altered inflammation in zebrafish larvae following embryonic glucocorticoid exposure, indicating receptor-mediated immune adaptation.

Key Points

To determine how elevated cortisol levels during early embryonic development alter immune function, leukocyte recruitment, and sepsis survival in zebrafish larvae.
Fertilized zebrafish eggs from AB and TL strains were treated with cortisol, dexamethasone (a selective glucocorticoid receptor agonist), or control medium from 0 to 6 hours post-fertilization (hpf).
Baseline expression of immune-related genes (socs3a, mpeg1.1, mpeg1.2, irg1l) was quantified at 5 days post-fertilization (dpf) across strains.
In AB strain larvae, leukocyte migration was tracked 4 hours after tail fin amputation at 3 dpf, and survival was tracked following exposure to 150 μg/ml lipopolysaccharide (LPS) at 4–5 dpf.
Cortisol and dexamethasone exposure markedly upregulated baseline expression of socs3a, mpeg1.1, mpeg1.2, and irg1l at 5 dpf in both AB and TL strains.
Dexamethasone significantly enhanced neutrophil migration to the wound site 4 hours after tail fin amputation, whereas early cortisol exposure did not alter recruitment.
Both early cortisol and dexamethasone treatments improved survival and reduced tail fin tissue damage following LPS challenge, accompanied by altered transcription of tlr4bb, cxcr4a, myd88, il1β, and il10.

Cite This Study

Bos et al. (2020) studied this question.

synapsesocial.com/papers/6aa14077b90bc0e4d272dbcd https://doi.org/10.3389/fimmu.2020.00727

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April 29, 2020Frontiers in ImmunologyOpen Access

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

View Full Paper

Ask AI

Bookmark

Authors

RBRuud van den Bos SCSuzanne Cromwijk KTKatharina Tschigg

Discussion

Member takes

Overview

Experimental study demonstrates enhanced sepsis survival and altered inflammation in zebrafish larvae following embryonic glucocorticoid exposure, indicating receptor-mediated immune adaptation.

Key Points

To determine how elevated cortisol levels during early embryonic development alter immune function, leukocyte recruitment, and sepsis survival in zebrafish larvae.
Fertilized zebrafish eggs from AB and TL strains were treated with cortisol, dexamethasone (a selective glucocorticoid receptor agonist), or control medium from 0 to 6 hours post-fertilization (hpf).
Baseline expression of immune-related genes (socs3a, mpeg1.1, mpeg1.2, irg1l) was quantified at 5 days post-fertilization (dpf) across strains.
In AB strain larvae, leukocyte migration was tracked 4 hours after tail fin amputation at 3 dpf, and survival was tracked following exposure to 150 μg/ml lipopolysaccharide (LPS) at 4–5 dpf.
Cortisol and dexamethasone exposure markedly upregulated baseline expression of socs3a, mpeg1.1, mpeg1.2, and irg1l at 5 dpf in both AB and TL strains.
Dexamethasone significantly enhanced neutrophil migration to the wound site 4 hours after tail fin amputation, whereas early cortisol exposure did not alter recruitment.
Both early cortisol and dexamethasone treatments improved survival and reduced tail fin tissue damage following LPS challenge, accompanied by altered transcription of tlr4bb, cxcr4a, myd88, il1β, and il10.

Cite This Study

Bos et al. (2020) studied this question.

synapsesocial.com/papers/6aa14077b90bc0e4d272dbcd https://doi.org/10.3389/fimmu.2020.00727

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