Evidence map›Paper›PMID 42064575›Full record

ArticleNeurobiology of stress2026

The role of proinflammatory response and the kynurenine pathway in the association between childhood maltreatment and lifetime substance use disorder.

Lars Östman, Elisabeth R Paul, He Zhang, Evelina Larsson, Irene Perini, Lilly Schwieler, Sophie Erhardt, Lovisa Holm, Åsa Axén, Leah M Mayo and 2 more

Abstract read
In one paragraph

Article in Neurobiology of stress, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Lars ÖstmanCenter for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Elisabeth R PaulCenter for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
He ZhangCenter for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Evelina LarssonDepartment of Psychiatry, Linköping, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Irene PeriniCenter for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Lilly SchwielerDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Sophie ErhardtDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Lovisa HolmCenter for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Åsa AxénCenter for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Leah M MayoCenter for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Markus HeiligCenter for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Andrea J CapusanCenter for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Childhood maltreatment (CM) is a risk factor for adult psychiatric and substance use disorders (SUD). Retrospectively assessed CM has been linked to increased proinflammatory cytokines, including IL-6. Induced by inflammation, the neurotoxic branch of the kynurenine pathway has been implicated in psychiatric disorders and SUD. This study explored proinflammatory responses and kynurenine metabolites following acute stress in participants with, and without, prospectively recorded CM, with or without, lifetime SUD. Methods: The study included 89 participants, divided into 4 groups based on the presence or absence of prospectively assessed CM and lifetime SUD: CM + SUD, n = 24, CM only, n = 20, SUD only, n = 22, and healthy controls (HC), n = 23. Participants underwent an acute stress task. Blood was collected at five time-points measuring IL-6 and kynurenine metabolites. Linear mixed models assessed the effects of CM, SUD, and time on IL-6 and kynurenine metabolite levels. Results: Participants with prospectively recorded CM had higher baseline IL-6 compared to those without CM (mean difference = 0.37, 95% CI = 0.09-0.57, p = 0.008). Stress increased IL-6 in all participants (p < 0.001), with no significant group differences. We found no association between CM exposure and KYNA or QUIN concentrations. Participants with SUD, irrespective of CM-status, had a lower KYNA/QUIN ratio (mean difference: 0.02, 95% CI: 0.00-0.04, p = 0.047). Discussion: Our findings of low-grade proinflammatory activity support the hypothesis that CM contributes to long-term immune system alterations, but these findings do not support the role of the kynurenine pathway in this process. However, increased neurotoxicity through kynurenine metabolism was associated to SUD-diagnosis.

Identifiers

PMID42064575
PMCPMC13127391

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.