Evidence map›Paper›PMID 27444789›Full record

ArticleBiology open2016

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

Ellen I Hartig, Shusen Zhu, Benjamin L King, James A Coffman

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.4field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Soy Isoflavones Induce Feminization of Japanese Eel (International journal of molecular sciences · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. The early function of cortisol in liver duringFrontiers in immunology · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Ellen I HartigMDI Biological Laboratory, Kathryn W. Davis Center for Regenerative Biology and Medicine, Salisbury Cove, ME, 04672, USA.
Shusen ZhuMDI Biological Laboratory, Kathryn W. Davis Center for Regenerative Biology and Medicine, Salisbury Cove, ME, 04672, USA.
Benjamin L KingMDI Biological Laboratory, Kathryn W. Davis Center for Regenerative Biology and Medicine, Salisbury Cove, ME, 04672, USA.
James A CoffmanMDI Biological Laboratory, Kathryn W. Davis Center for Regenerative Biology and Medicine, Salisbury Cove, ME, 04672, USA jcoffman@mdibl.org.ORCID http://orcid.org/0000-0001-8536-3844
Mount Desert Island Biological Laboratory · US

Funding

The Maine Biomedical Research Network (INBRE)P20GM103423 · NIGMS · MOUNT DESERT ISLAND BIOLOGICAL LAB · PI Dustin Lynn Updike · 2012 to 2026
$60.0M
Understanding the role of thyroid hormone signaling during axolotl limb regenerationP20GM104318 · NIGMS · MOUNT DESERT ISLAND BIOLOGICAL LAB · PI DRUMMOND, IAIN A. · 2013 to 2023
$23.0M
NIGMS NIH HHS P20 GM103423NIGMS NIH HHS P20 GM104318
6 · The paper itself

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 both larvae and adults. Treated larvae had elevated whole-body cortisol and glucocorticoid signaling, and upregulated genes associated with defense response and immune system processes. 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.

Indexed as

Chronic stressDevelopmental programmingGlucocorticoidImmune systemRNA-seqZebrafish

Identifiers

PMID27444789
PMCPMC5004618
OpenAlexW2478730098

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.