The following is a summary of “Association between microbiome and the development of adverse posttraumatic neuropsychiatric sequelae after traumatic stress exposure,” published in the November 2023 issue of Psychiatry by Zeamer et al.
Adverse post-traumatic neuropsychiatric sequelae (APNS) frequently afflict trauma-exposed patients, yet the biological mechanisms fostering these outcomes remain elusive. The microbiota-gut-brain axis presents a promising avenue for comprehending these mechanisms and potential interventions. However, the examination of post-trauma microbiome compositions concerning neuropsychiatric effects remains limited. In this investigation, as part of the Advancing Understanding of RecOvery after traumA (AURORA) study, metagenomic analysis was conducted on stool samples from 51 adults post-trauma to probe potential dysfunctions within gut microbiome profiles and explore associated mechanisms.
Assessments at two, eight, and twelve weeks post-trauma encompassed post-traumatic stress disorder (PTSD) evaluations using the PTSD checklist for DSM-5, normalized depression scores (PROMIS Depression Short Form 8b), and somatic symptom counts. Generalized linear models incorporating microbial abundances and pertinent demographics were constructed for each outcome. Furthermore, mixed-effect random forest machine learning models were utilized to unveil associations between APNS outcomes and microbial features and encoded metabolic pathways derived from stool metagenomics.
Several microbial species, notably Flavonifractor plautii, Ruminococcus gnavus, and diverse Bifidobacterium species, typical commensal gut microbes, emerged as significant predictors of adverse APNS outcomes based on microbial abundance data. Moreover, modeling APNS outcomes using microbial metabolic pathways unveiled a noteworthy prediction of worse APNS outcomes linked to decreased genes associated with the L-arginine way and increased citrulline and ornithine pathways. Notably, common commensal microbial species were enriched among individuals developing APNS. Crucially, a potential biological mechanism was identified, suggesting that the gut microbiome may curtail global arginine bioavailability, a metabolic change similarly observed in the plasma of PTSD patients.
These findings emphasize the relevance of investigating gut microbiome alterations in APNS development, offering potential avenues for therapeutic interventions and deeper insights into post-trauma neuropsychiatric outcomes. Further exploration of these microbial signatures and pathways holds promise for refining interventions targeting trauma-induced neuropsychiatric complications.