Cited by 54Tryptophan and brain disordersStress Responses and CortisolTreatment of Major Depression

Transcriptomic predictors of inflammation-induced depressed mood

Open access
Cho, Joshua Hyong-Jin, Irwin, Michael R., Eisenberger, Naomi I., Lamkin, Donald M., Cole, Steve W.·2019·Neuropsychopharmacology

Abstract

Inflammation plays a significant role in the pathophysiology of depression. However, not all individuals exposed to inflammatory challenge develop depression, and identifying those at risk is necessary to develop targeted monitoring, prevention, and treatment strategies. Within a randomized double-blind placebo-controlled study (n = 115), we examined whether leukocyte transcriptome profiles predicted inflammation-induced depressed mood in volunteers who received low-dose intravenous endotoxin (n = 58; aged 18-50). At baseline, transcription factor (TF) activities were assessed using genome-wide transcriptional profiling of peripheral blood mononuclear cells and promoter-based bioinformatic analyses. Then, participants were administered endotoxin. Self-reported depressed mood was assessed using the Profile of Mood States. Based on extant studies linking transcriptional profiles to depressive disorder, we examined whether post-endotoxin depressed mood is predicted by baseline activity of TFs related to immune activation, sympathetic activation, and glucocorticoid insensitivity: respectively, nuclear factor kappa B (NF-kB), cAMP response element-binding protein (CREB), and glucocorticoid receptor (GR). Twenty-one participants (36%) experienced an increase in depressed mood from baseline to 2 h post endotoxin, when depressive response peaks. Bioinformatics analyses controlling for age, sex, ethnicity, body mass index, and physical sickness response revealed that post-endotoxin depressed mood was predicted by increased baseline activity of TFs related to inflammation (NF-kB) and beta-adrenergic signaling (CREB) and by decreased activity of GR-related TFs (P's < 0.001). Inflammation-induced depressed mood is predicted by peripheral transcriptome profiles related to immune activation, sympathetic activation, and glucocorticoid insensitivity. With further replication, these stress-related molecular profiles could be used for a novel genomic approach for identifying individuals at high-risk for the inflammatory subtype of depression.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/s41386-019-0316-9

Cites

55 of 55 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Inflammation-induced depressed mood can be predicted by elevated blood mononuclear cell transcription factor activity related to immune activation (NFκB), sympathetic activation, and glucocorticoid insensitivity.

    “Inflammation-induced depressed mood can be predicted by elevated blood mononuclear cell transcription factor activity related to immune activation (NFκB), sympathetic activation, and glucocorticoid (GC) insensitivity [62].”

    From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [62]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

4 of the 59 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Cho, J. H.-J., Irwin, M. R., Eisenberger, N. I., Lamkin, D. M., & Cole, S. W.
Affiliations
University of California, Los Angeles (US)
Venue
Neuropsychopharmacology
Published
2019-01-14
Volume
44
Issue
5
Pages
923-929
ISSN
  • 0893-133X (ISSN-L)
  • 1740-634X
OpenAlex
W2909111591
Cited by
54
References
59
Citations by year
2026: 8 · 2025: 6 · 2024: 10 · 2023: 7 · 2022: 7 · 2021: 9 · 2020: 3 · 2019: 4
FWCI
1.89
Type
journal article
Language
en
Open access
Locations
  • Neuropsychopharmacology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (5R01MH091352)
  • U.S. Department of Health & Human Services | NIH | National Institute on Aging (K23AG049085)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Keywords
depressive mood, endotoxin challenge, leukocyte transcriptome, transcription factor activity, NF-kB, CREB, glucocorticoid receptor, glucocorticoid resistance, beta-adrenergic signaling, immune activation, peripheral blood mononuclear cells, risk prediction
MeSH terms
Adolescent, Adult, Depression, Double-Blind Method, Endotoxins, Female, Humans, Inflammation, Leukocytes, Mononuclear, Male, Middle Aged, Receptors, Glucocorticoid, NF-kappa B, Computational Biology, CREB-Binding Protein, Young Adult, Transcriptome

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review