TY - JOUR
T1 - Association of T and non-T cell cytokines with anhedonia
T2 - Role of gender differences
AU - Jha, Manish K.
AU - Miller, Andrew H.
AU - Minhajuddin, Abu
AU - Trivedi, Madhukar H.
N1 - Funding Information:
Drs. Miller and Minhajuddin have no potential conflicts of interest. Dr. Jha has received contract research support from Acadia Pharmaceuticals and Janssen . Dr. Trivedi is or has been an advisor/consultant and received fees from Alkermes, AstraZeneca, Cerecor, Eli Lilly & Company, Lundbeck, Naurex, Neuronetics, Otsuka Pharmaceuticals, Pamlab, Pfizer Inc., SHIRE Development and Takeda. In addition, he has received grants/research support from National Institute of Mental Health and National Institute on Drug Abuse .
Funding Information:
The CO-MED trial was funded by 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). This work was also supported in part through the Center for Depression Research and Clinical Care at UT Southwestern (Principal Investigator: Madhukar H. Trivedi, MD) and Hersh Foundation . The authors thank the clinical staff at each clinical site for their assistance with this project; all of the study participants; and Jeremy Kee, M.A. for administrative support. Forest Pharmaceuticals, GlaxoSmithKline, Organon, and Wyeth Pharmaceuticals provided medications for CO-MED trial at no cost. 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:
© 2018
PY - 2018/9
Y1 - 2018/9
N2 - Objective: Among individual depressive symptoms, anhedonia has been reliably associated with activation of the innate immune response. However, it is unclear whether this association extends to T cell cytokines and if gender differentially affects this association. Method: Concentrations of T (IL-17, T-helper (Th) 1- and Th2-) and non-T cell cytokines were measured in plasma using the Bioplex Pro™ human cytokine multiplex kit in Combining Medications to Enhance Depression Outcomes (CO-MED) trial participants who provided plasma at baseline (n = 166). Anhedonia was measured with three items of the clinician-rated Inventory of Depressive Symptomatology and depression severity (minus anhedonia item) was measured with Quick Inventory of Depression Severity Self-Report version (modified-QIDS-SR). Separate generalized linear models for anhedonia and modified-QIDS-SR as dependent variables were conducted with IL-17, Th1-, Th2-, and non-T cell- cytokines as primary independent variables and gender, body mass index (BMI), and age as covariates. Exploratory analyses included gender-by-biomarker interactions. Results: Higher levels of IL-17 (p = 0.032), Th1- (p = 0.002), Th2-(p = 0.001) and non-T-(p = 0.009) cell markers were associated with greater severity of anhedonia controlling for BMI, age, and gender. Gender also had a significant main effect on anhedonia, however, there was a significant gender by immune marker interaction only for IL-17 (p = 0.050). Anhedonia severity increased with higher IL-17 in males (r = 0.42, p = 0.003) but not in females (r = 0.09, p = 0.336). Only non-T cell markers were associated with the modified-QIDS-SR, and there were no significant gender-specific associations with this variable. Conclusions: T and non-T cell-related inflammatory markers were associated with greater severity of anhedonia, while gender moderated the association of IL-17 with anhedonia in patients with major depressive disorder.
AB - Objective: Among individual depressive symptoms, anhedonia has been reliably associated with activation of the innate immune response. However, it is unclear whether this association extends to T cell cytokines and if gender differentially affects this association. Method: Concentrations of T (IL-17, T-helper (Th) 1- and Th2-) and non-T cell cytokines were measured in plasma using the Bioplex Pro™ human cytokine multiplex kit in Combining Medications to Enhance Depression Outcomes (CO-MED) trial participants who provided plasma at baseline (n = 166). Anhedonia was measured with three items of the clinician-rated Inventory of Depressive Symptomatology and depression severity (minus anhedonia item) was measured with Quick Inventory of Depression Severity Self-Report version (modified-QIDS-SR). Separate generalized linear models for anhedonia and modified-QIDS-SR as dependent variables were conducted with IL-17, Th1-, Th2-, and non-T cell- cytokines as primary independent variables and gender, body mass index (BMI), and age as covariates. Exploratory analyses included gender-by-biomarker interactions. Results: Higher levels of IL-17 (p = 0.032), Th1- (p = 0.002), Th2-(p = 0.001) and non-T-(p = 0.009) cell markers were associated with greater severity of anhedonia controlling for BMI, age, and gender. Gender also had a significant main effect on anhedonia, however, there was a significant gender by immune marker interaction only for IL-17 (p = 0.050). Anhedonia severity increased with higher IL-17 in males (r = 0.42, p = 0.003) but not in females (r = 0.09, p = 0.336). Only non-T cell markers were associated with the modified-QIDS-SR, and there were no significant gender-specific associations with this variable. Conclusions: T and non-T cell-related inflammatory markers were associated with greater severity of anhedonia, while gender moderated the association of IL-17 with anhedonia in patients with major depressive disorder.
KW - Anhedonia
KW - Depression
KW - Gender
KW - Inflammation
KW - Interleukin 17
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U2 - 10.1016/j.psyneuen.2018.05.017
DO - 10.1016/j.psyneuen.2018.05.017
M3 - Article
C2 - 29783087
AN - SCOPUS:85047096990
VL - 95
SP - 1
EP - 7
JO - Psychoneuroendocrinology
JF - Psychoneuroendocrinology
SN - 0306-4530
ER -