TY - JOUR
T1 - Proteomics profiling reveals inflammatory biomarkers of antidepressant treatment response
T2 - Findings from the CO-MED trial
AU - Gadad, Bharathi S.
AU - Jha, Manish K.
AU - Grannemann, Bruce D.
AU - Mayes, Taryn L.
AU - Trivedi, Madhukar H.
N1 - Funding Information:
The authors thank the clinical staff at each clinical site, including site investigators and co-investigators for their assistance with this project; all of the study participants; and Jennifer Furman, Ph.D. for her extensive editorial and administrative contributions. This work was supported by the National Institute of Mental Health under contract N01 MH-90003 to the University of Texas Southwestern Medical Center at Dallas (principal investigators, M.H. Trivedi and A.J. Rush). Forest Pharmaceuticals, GlaxoSmithKline, Organon, and Wyeth Pharmaceuticals provided medications for this trial at no cost. This work was also supported in part through the Center for Depression Research and Clinical Care (Principal Investigator: Madhukar H. Trivedi, MD) and Hersh Foundation (MHT). The content of this publication does not necessarily reflect the views or policies of the U.S. Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. government. NIMH had no role in the drafting or review of the manuscript or in the collection or analysis of the data.
Publisher Copyright:
© 2017 Elsevier Ltd
PY - 2017/11
Y1 - 2017/11
N2 - Animal and human studies suggest an association between depression and aberrant immune response. Further, common inflammatory markers may change during the course of antidepressant treatment in patients. The objective of this study was to evaluate changes in inflammatory markers and clinical outcomes from subjects enrolled in the Combining Medications to Enhance Depression Outcome (CO-MED) trial. At baseline and week 12 (treatment completion), plasma samples of 102 participants were analyzed via a multiplex assay comprised of inflammatory markers using a 27-plex standard assay panel plus a 4-plex human acute phase xMAP technology based platform. We carried out analyses in two steps. First, t-tests were used to identify inflammatory marker levels that changed between baseline and week 12. For markers that were altered, logistic regression models were then conducted to look for associated changes in remission at week 12. Among the 31 inflammatory markers analyzed, several cytokines (IL-5, IFN-γ, IL-13), two chemokines (Eotaxin-1/CCL11, RANTES) and an acute-phase reactant (serum amyloid P component) showed change from baseline to week 12. However, only two indicated differential remission responses. Interestingly, increased levels of Eotaxin-1/CCL11 correlated with remission at week 12, whereas decreased levels of IFN-γ correlated with non-remission at week 12. Results suggest that these inflammatory proteins may serve as predictors of treatment response.
AB - Animal and human studies suggest an association between depression and aberrant immune response. Further, common inflammatory markers may change during the course of antidepressant treatment in patients. The objective of this study was to evaluate changes in inflammatory markers and clinical outcomes from subjects enrolled in the Combining Medications to Enhance Depression Outcome (CO-MED) trial. At baseline and week 12 (treatment completion), plasma samples of 102 participants were analyzed via a multiplex assay comprised of inflammatory markers using a 27-plex standard assay panel plus a 4-plex human acute phase xMAP technology based platform. We carried out analyses in two steps. First, t-tests were used to identify inflammatory marker levels that changed between baseline and week 12. For markers that were altered, logistic regression models were then conducted to look for associated changes in remission at week 12. Among the 31 inflammatory markers analyzed, several cytokines (IL-5, IFN-γ, IL-13), two chemokines (Eotaxin-1/CCL11, RANTES) and an acute-phase reactant (serum amyloid P component) showed change from baseline to week 12. However, only two indicated differential remission responses. Interestingly, increased levels of Eotaxin-1/CCL11 correlated with remission at week 12, whereas decreased levels of IFN-γ correlated with non-remission at week 12. Results suggest that these inflammatory proteins may serve as predictors of treatment response.
KW - Antidepressant
KW - Cytokine
KW - Eotaxin-1/CCL11
KW - IFN-γ
KW - Multiplex
KW - Predictor
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U2 - 10.1016/j.jpsychires.2017.05.012
DO - 10.1016/j.jpsychires.2017.05.012
M3 - Article
C2 - 28628884
AN - SCOPUS:85020913161
SN - 0022-3956
VL - 94
SP - 1
EP - 6
JO - Journal of Psychiatric Research
JF - Journal of Psychiatric Research
ER -