Transcriptional signatures related to glucose and lipid metabolism predict treatment response to the tumor necrosis factor antagonist infliximab in patients with treatment-resistant depression
Open accessAbstract
The tumor necrosis factor (TNF) antagonist infliximab was recently found to reduce depressive symptoms in patients with increased baseline inflammation as reflected by a plasma C-reactive protein concentration >5 mg/L. To further explore predictors and targets of response to infliximab, differential gene expression was examined in peripheral blood mononuclear cells from infliximab responders (n=13) versus non-responders (n=14) compared to placebo at baseline and 6 h, 24 h, and 2 weeks after the first infliximab infusion. Treatment response was defined as 50% reduction in depressive symptoms at any point during the 12-week trial. One-hundred-forty-eight gene transcripts were significantly associated (1.2-fold, adjusted p≤0.01) with response to infliximab and were distinct from placebo responders. Transcripts predictive of infliximab response were associated with gluconeogenesis and cholesterol transport, and were enriched in a network regulated by hepatocyte nuclear factor (HNF)4-alpha, a transcription factor involved in gluconeogenesis and cholesterol and lipid homeostasis. Of the 148 transcripts differentially expressed at baseline, 48% were significantly regulated over time in infliximab responders, including genes related to gluconeogenesis and the HNF4-alpha network, indicating that these predictive genes were responsive to infliximab. Responders also demonstrated inhibition of genes related to apoptosis through TNF signaling at 6 h and 24 h after infusion. Transcripts down-regulated in responders 2 weeks after infliximab were related to innate immune signaling and nuclear factor-kappa B. Thus, baseline transcriptional signatures reflective of alterations in glucose and lipid metabolism predicted antidepressant response to infliximab, and infliximab response involved regulation of metabolic genes and inhibition of genes related to innate immune activation.
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Self-citation
- Authors
- Mehta, D., Raison, C. L., Woolwine, B. J., Haroon, E., Binder, E. B., Miller, A. H., & Felger, J. C.
- Affiliations
- Max Planck Institute of Psychiatry (DE)
- University of Arizona (US)
- Emory University (US)
- Corresponding author
- Felger, Jennifer C.
- ORCID
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2013-07
- Volume
- 31
- Pages
- 205-215
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC3673885
- OpenAlex
- W2054093295
- Cited by
- 74
- References
- 73
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 6 · 2022: 9 · 2021: 8 · 2020: 5 · 2019: 4 · 2018: 4 · 2017: 1 · 2016: 8 · 2015: 7 · 2014: 6 · 2013: 4
- FWCI
- 2.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- National Institutes of Health (UL1TR000454, UL1TR002378)
- National Institute of Mental Health (R21MH077172, R21 MH0771172, R03MH100273, R01MH108605, R01MH109637, R01MH087604)
- National Cancer Institute (P30CA138292)
- National Center for Research Resources (UL1RR025008, M01RR000039, M01-RR-0039)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- infliximab, treatment-resistant depression, tumor necrosis factor inhibitors, treatment response prediction, gene expression signatures, glucose metabolism, lipid metabolism, gluconeogenesis, cholesterol transport, peripheral blood mononuclear cells, inflammation, C-reactive protein, apoptosis, innate immune signaling, NF-κB, TNF signaling
- MeSH terms
- Infliximab, Adult, Antibodies, Monoclonal, Antidepressive Agents, Double-Blind Method, Female, Glucose, Humans, Male, Middle Aged, Tumor Necrosis Factor-alpha, Treatment Outcome, Gene Expression Profiling, Carbohydrate Metabolism, Lipid Metabolism, Depressive Disorder, Treatment-Resistant
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 ›
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