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Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation [adults]

ABSTRACT: Chronic early life stress increases adult susceptibility to numerous health problems linked to chronic inflammation. One way that this may occur is via glucocorticoid-induced developmental programming. To gain insight into such programming, we treated zebrafish embryos with cortisol and examined the effects on adults. In adulthood, the treated fish maintained elevated basal cortisol levels in the absence of exogenous cortisol, and constitutively mis-expressed genes involved in defense response and its regulation. Adults derived from cortisol-treated embryos displayed defective tailfin regeneration, heightened basal expression of pro-inflammatory genes, and failure to appropriately regulate those genes following injury or immunological challenge. These results support the hypothesis that chronically elevated glucocorticoid signaling early in life directs development of a pro-inflammatory adult phenotype, at the expense of immunoregulation and somatic regenerative capacity.

ORGANISM(S): Danio rerio

PROVIDER: GSE80260 | GEO | 2016/06/01

SECONDARY ACCESSION(S): PRJNA318414

REPOSITORIES: GEO

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Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation [adults]

Project description:Chronic early life stress increases adult susceptibility to numerous health problems linked to chronic inflammation. One way that this may occur is via glucocorticoid-induced developmental programming. To gain insight into such programming, we treated zebrafish embryos with cortisol and examined the effects on adults. In adulthood, the treated fish maintained elevated basal cortisol levels in the absence of exogenous cortisol, and constitutively mis-expressed genes involved in defense response and its regulation. Adults derived from cortisol-treated embryos displayed defective tailfin regeneration, heightened basal expression of pro-inflammatory genes, and failure to appropriately regulate those genes following injury or immunological challenge. These results support the hypothesis that chronically elevated glucocorticoid signaling early in life directs development of a pro-inflammatory adult phenotype, at the expense of immunoregulation and somatic regenerative capacity. 30 samples total were analyzed. 9 caudal fins samples (0, 2 and 4dpa), 3 blood samples and 3 muscle samples from adults exposed to DMSO control as embryos. 9 caudal fins samples (0, 2 and 4dpa), 3 blood samples and 3 muscle samples from adults exposed to cortisol (1 micromolar) as embryos.

2016-06-01 | E-GEOD-80260 | biostudies-arrayexpress

Chronic glucocorticoid exposure in early development leads to neuroendocrine, metabolic, and immune dysregulation in adult zebrafish

Project description:Chronic early life stress can affect development of the neuroendocrine stress system, leading to its persistent dysregulation and consequently increased disease risk in adulthood. One contributing factor is thought to be epigenetic programming in response to chronic glucocorticoid exposure during early development. We have previously shown that zebrafish embryos treated chronically with cortisol develop into adults with constitutively elevated whole body cortisol and aberrant immune gene expression. The objective of the experiments reported here was to further characterize the phenotype of those adults. We find that adult zebrafish derived from cortisol-treated embryos have aberrant cortisol tissue distribution and dynamics, which correlate with differential transcriptional activity of key glucocorticoid-responsive regulatory genes klf9 and fkbp5 in blood and brain.

2019-10-28 | GSE137987 | GEO

Response to low-dose cortisol treatment in zebrafish embryos [larvae]

2016-06-01 | E-GEOD-80221 | biostudies-arrayexpress

Response to low-dose cortisol treatment in zebrafish embryos [larvae]

2016-06-01 | GSE80221 | GEO

Investigation of gene expression responses to acute stress exposure in adults with early childhood adversity experience

Project description:Exposure to serious or traumatic events early in life can lead to persistent alterations in physiological stress response systems, including enhanced cross-talk between the neuroendocrine and immune system. These programming effects may be mechanistically involved in mediating the effects of adverse childhood experience on disease risk in adulthood. Here, we investigated neuroendocrine as well as genome-wide mRNA expression responses in monocytes to acute stress exposure, in a sample of healthy adults (n=30) with a history of early childhood adversity, and a control group (n=30) without trauma experience. The early adversity group showed altered hypothalamus-pituitary-adrenal (HPA) axis responses to stress, evidenced by lower ACTH and cortisol responses. Analyses of gene expression patterns showed a larger stress-induced increase of cardinal pro-inflammatory transcripts IL6 and FOSB, and an increased activity of pro-inflammatory upstream signaling in the early adversity group. We also identified transcripts that were differentially correlated with stress-induced cortisol increases between the groups. Noteworthy, FKBP5 expression was less responsive to cortisol induction in the early adversity group, with potential effects on the ultra-short feedback loop that balances FKBP5 and glucocorticoid receptor activity. Further exploratory analyses showed differential stress-induced regulation of gene transcription between the groups. Prominent among the differentially regulated transcripts were those coding for genes involved in signal transducer activity, G-protein coupled receptors, and several genes involved in serotonin receptor signaling. We suggest that childhood adversity leads to persistent alterations in transcriptional control of stress responsive pathways, which - when chronically or repeatedly activated - might predispose individuals to stress-related psychopathology.

2015-11-30 | GSE70603 | GEO

Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation

Project description:Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation

| PRJNA318502 | ENA

Danio rerio

Project description:Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation [adults]

| PRJNA318414 | ENA

Effects of egg enrichment with glucocorticoid hormone, antagonist and receptor messenger in the modulation of gene expression in zebrafish (Danio rerio) embryos

Project description:Several studies have shown the presence of large reservoirs of maternally contributed liposoluble hormones in the yolk of mature teleost oocytes, such as steroid, thyroid and retinoid hormones, as found in other oviparous vertebrates. This supports the idea that maternal hormones could play a major role in regulating developmental processes post-fertilization. The aims of this study were: A) to verify whether a cortisol treatment of zebrafish eggs affects the growth rate of the progenies as compared to controls in F1-F4 treated generations (ontogenetic programming). It was to be established whether: 1) this is due to a short-term effect of maternal cortisol, directly producing an initial growth retard that is not compensated later on in lifetime (short-term epigenetic effect); or 2) this is due to a long-term priming of growth rate by maternal cortisol that persists later on in lifetime (long-term epigenetic effect); B) to verify whether the ontogenetic programming is inheritable, being transmitted also to the untreated F4 generation. It was to be established whether the programmed genes are developmental and/or growth genes that are inhibited, or genes encoding hormones of the corticoid stress axis (hypothalamo-hypophyso-interrenal axis) that are amplified, or both gene clusters. Control embryos (treated with the vehicle ethanol only) were compared to cortisol-treated embryos at 5 hpf, 12 hpf and 24 hpf. Four replicates were performed for the 5 hpf samples, three biological replicates were carried out for the 12 hpf samples, and a single experiment was performed for the 24 hpf samples.

2016-07-03 | E-GEOD-52398 | biostudies-arrayexpress

Transcription profiling of human HeLa cells treated by various doses of cortisol

Project description:Glucocorticoids act through the glucocorticoid receptor (GR), a ligand activated transcription factor, to modulate gene expression profiles in target cells and tissues. The principal physiological glucocorticoid in humans, cortisol, is released in a pulsatile fashion from the adrenal gland, which results in oscillations in blood concentrations, with a period of 1 - 2 hours. The biological consequence of fluctuating cortisol concentrations has not been explored. To identify the role of cortisol concentration oscillations for target cell response a flow-through cell culture system was developed. Transcription profiling was performed in the absence and presence of cortisol. Cells were exposed to constant cortisol levels of 100ng/ml or 200 ng/ml or oscillating cortisol concentrations.

2010-07-10 | E-MEXP-2447 | biostudies-arrayexpress

Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [ATAC-seq]

Project description:Early life environmental exposure, particularly during perinatal period, can have a lifelong impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptation to the anticipated environment based on early life experience. However, perinatal exposure to adverse environments can also be associated with adult-onset disorders. Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their role in developmental programming. Here, we report that perinatal glucocorticoid exposure had long-term consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tumor growth and bacterial infection. We found that perinatal glucocorticoid exposure resulted in persistent alteration of the hypothalamic-pituitaryadrenal (HPA) axis. Consequently, the level of the hormone in adults was significantly reduced, resulting in decreased CD8 T cell function. Our study thus demonstrates that perinatal stress can have long-term consequences on CD8 T cell immunity by altering HPA axis activity.

2020-01-01 | GSE136972 | GEO

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