PTSD is associated with neuroimmune suppression: evidence from PET imaging and postmortem transcriptomic studies

Shivani Bhatt, Ansel T. Hillmer, Matthew J. Girgenti, Aleksandra Rusowicz, Michael Kapinos, Nabeel Nabulsi, Yiyun Huang, David Matuskey, Gustavo A. Angarita, Irina Esterlis, Margaret T. Davis, Steven M. Southwick, Matthew J. Friedman, Ronald S. Duman, Richard E. Carson, John H. Krystal, Robert H. Pietrzak and Kelly P. Cosgrove ()
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Shivani Bhatt: Yale University
Ansel T. Hillmer: Yale School of Medicine
Matthew J. Girgenti: Yale School of Medicine
Aleksandra Rusowicz: Yale School of Medicine
Michael Kapinos: Yale School of Medicine
Nabeel Nabulsi: Yale School of Medicine
Yiyun Huang: Yale School of Medicine
David Matuskey: Yale School of Medicine
Gustavo A. Angarita: Yale School of Medicine
Irina Esterlis: Yale University
Margaret T. Davis: Yale School of Medicine
Steven M. Southwick: Yale School of Medicine
Matthew J. Friedman: Dartmouth Medical School
Ronald S. Duman: Yale School of Medicine
Richard E. Carson: Yale School of Medicine
John H. Krystal: Yale School of Medicine
Robert H. Pietrzak: Yale School of Medicine
Kelly P. Cosgrove: Yale University

Nature Communications, 2020, vol. 11, issue 1, 1-11

Abstract: Abstract Despite well-known peripheral immune activation in posttraumatic stress disorder (PTSD), there are no studies of brain immunologic regulation in individuals with PTSD. [11C]PBR28 Positron Emission Tomography brain imaging of the 18-kDa translocator protein (TSPO), a microglial biomarker, was conducted in 23 individuals with PTSD and 26 healthy individuals—with or without trauma exposure. Prefrontal-limbic TSPO availability in the PTSD group was negatively associated with PTSD symptom severity and was significantly lower than in controls. Higher C-reactive protein levels were also associated with lower prefrontal-limbic TSPO availability and PTSD severity. An independent postmortem study found no differential gene expression in 22 PTSD vs. 22 controls, but showed lower relative expression of TSPO and microglia-associated genes TNFRSF14 and TSPOAP1 in a female PTSD subgroup. These findings suggest that peripheral immune activation in PTSD is associated with deficient brain microglial activation, challenging prevailing hypotheses positing neuroimmune activation as central to stress-related pathophysiology.

Date: 2020
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DOI: 10.1038/s41467-020-15930-5

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