Depressive Symptoms in Patients with Chronic Hepatitis C Are Correlated with Elevated Plasma Levels of Interleukin-1beta and Tumor Necrosis Factor-alpha

Overview

Journal Neurosci Lett

Specialty Neurology

Date 2007 Dec 8

PMID 18063307

Citations 55

Authors

Jennifer M Loftis

Marilyn Huckans

Samantha Ruimy

David J Hinrichs

Peter Hauser

Affiliations

Soon will be listed here.

Abstract

Studies suggest that cytokines have a role in the biology of depression. In this study, we evaluated depression and cytokine levels in patients with and without chronic hepatitis C (HCV) to better assess how chronic infection alters cytokines levels and may contribute to depressive symptomotology. Twenty-three adults with (n=16) and without (n=7) HCV were recruited through the Portland VA Medical Center. Research participants were excluded for current substance abuse, psychotic disorder, liver cirrhosis, or interferon (IFN) therapy. Participants completed the Beck Depression Inventory-II (BDI-II) and a blood draw to evaluate plasma cytokine levels [i.e., interleukin (IL)-1beta, IL-10 and tumor necrosis factor (TNF)-alpha]. t-Tests were performed to compare cytokine levels in patients with or without HCV. HCV patients showed higher TNF-alpha values compared to patients without HCV (group means=7.94 vs. 3.41pg/mL, respectively, p=0.047). There were no significant differences between the groups for the other cytokines assessed. In patients with HCV, TNF-alpha and IL-1beta levels (but not IL-10) were correlated with BDI-II scores [r=0.594, p=0.020 and r=0.489, p=0.055 (trend), respectively]. Taken together, these results show an association between severity of depressive symptoms and expression of pro-inflammatory cytokines in patients with HCV. Future studies should investigate how inflammatory mediators play a role in the expression of specific depressive symptoms in patients with chronic infection. Patients with HCV represent an interesting model to examine this relationship.

Citing Articles

Inflammatory and mental health sequelae of COVID-19.

Loftis J, Firsick E, Shirley K, Adkins J, Le-Cook A, Sano E Compr Psychoneuroendocrinol. 2023; 15:100186.

PMID: 37223650 PMC: 10191701. DOI: 10.1016/j.cpnec.2023.100186.

Lipocalin-2 Secreted by the Liver Regulates Neuronal Cell Function Through AKT-Dependent Signaling in Hepatic Encephalopathy Mouse Model.

Jo D, Jung Y, Song J Clin Nutr Res. 2023; 12(2):154-167.

PMID: 37214781 PMC: 10193436. DOI: 10.7762/cnr.2023.12.2.154.

Risk Factors of Severe COVID-19: A Review of Host, Viral and Environmental Factors.

Zsichla L, Muller V Viruses. 2023; 15(1).

PMID: 36680215 PMC: 9863423. DOI: 10.3390/v15010175.

A spotlight on HCV and SARS-CoV-2 co-infection and brain function.

Shirley K, Loftis J Pharmacol Biochem Behav. 2022; 217:173403.

PMID: 35561837 PMC: 9088049. DOI: 10.1016/j.pbb.2022.173403.

Selenium reduces nociceptive response in acute 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced neurotoxicity.

Abolarin P, Nafiu A, Oyewole A, Amin A, Ogundele O, Owoyele B IBRO Neurosci Rep. 2021; 12:1-11.

PMID: 34927129 PMC: 8652001. DOI: 10.1016/j.ibneur.2021.11.001.

References

Simen B, Duman C, Simen A, Duman R . TNFalpha signaling in depression and anxiety: behavioral consequences of individual receptor targeting. Biol Psychiatry. 2006; 59(9):775-85. DOI: 10.1016/j.biopsych.2005.10.013. View

Cozzi A, Zignego A, Carpendo R, Biagiotti T, Aldinucci A, Monti M . Low serum tryptophan levels, reduced macrophage IDO activity and high frequency of psychopathology in HCV patients. J Viral Hepat. 2006; 13(6):402-8. DOI: 10.1111/j.1365-2893.2005.00706.x. View

Dunn R, Kimbrell T, Ketter T, Frye M, Willis M, Luckenbaugh D . Principal components of the Beck Depression Inventory and regional cerebral metabolism in unipolar and bipolar depression. Biol Psychiatry. 2002; 51(5):387-99. DOI: 10.1016/s0006-3223(01)01244-6. View

OMahony S, Myint A, van den Hove D, Desbonnet L, Steinbusch H, Leonard B . Gestational stress leads to depressive-like behavioural and immunological changes in the rat. Neuroimmunomodulation. 2006; 13(2):82-8. DOI: 10.1159/000096090. View

Astle F . Diabetes and depression: a review of the literature. Nurs Clin North Am. 2007; 42(1):67-78, vii. DOI: 10.1016/j.cnur.2006.11.007. View

Licinio J, Wong M . The role of inflammatory mediators in the biology of major depression: central nervous system cytokines modulate the biological substrate of depressive symptoms, regulate stress-responsive systems, and contribute to neurotoxicity and neuroprotection. Mol Psychiatry. 1999; 4(4):317-27. DOI: 10.1038/sj.mp.4000586. View

Loftis J, Socherman R, Howell C, Whitehead A, Hill J, Dominitz J . Association of interferon-alpha-induced depression and improved treatment response in patients with hepatitis C. Neurosci Lett. 2004; 365(2):87-91. DOI: 10.1016/j.neulet.2004.04.058. View

Kraus M, Schafer A, Csef H, Scheurlen M, Faller H . Emotional state, coping styles, and somatic variables in patients with chronic hepatitis C. Psychosomatics. 2000; 41(5):377-84. DOI: 10.1176/appi.psy.41.5.377. View

Capuron L, Ravaud A, Neveu P, Miller A, Maes M, Dantzer R . Association between decreased serum tryptophan concentrations and depressive symptoms in cancer patients undergoing cytokine therapy. Mol Psychiatry. 2002; 7(5):468-73. DOI: 10.1038/sj.mp.4000995. View

10.

Loftis J, Hauser P . The phenomenology and treatment of interferon-induced depression. J Affect Disord. 2004; 82(2):175-90. DOI: 10.1016/j.jad.2004.04.002. View

11.

Wichers M, Koek G, Robaeys G, Verkerk R, Scharpe S, Maes M . IDO and interferon-alpha-induced depressive symptoms: a shift in hypothesis from tryptophan depletion to neurotoxicity. Mol Psychiatry. 2004; 10(6):538-44. DOI: 10.1038/sj.mp.4001600. View

12.

Maes M, Bosmans E, Meltzer H, Scharpe S, Suy E . Interleukin-1 beta: a putative mediator of HPA axis hyperactivity in major depression?. Am J Psychiatry. 1993; 150(8):1189-93. DOI: 10.1176/ajp.150.8.1189. View

13.

Ranjit N, Diez-Roux A, Shea S, Cushman M, Seeman T, Jackson S . Psychosocial factors and inflammation in the multi-ethnic study of atherosclerosis. Arch Intern Med. 2007; 167(2):174-81. DOI: 10.1001/archinte.167.2.174. View

14.

Voss J, Dodd M, Portillo C, Holzemer W . Theories of fatigue: application in HIV/AIDS. J Assoc Nurses AIDS Care. 2006; 17(1):37-50. DOI: 10.1016/j.jana.2005.11.004. View

15.

Hauser P, Khosla J, Aurora H, Laurin J, Kling M, Hill J . A prospective study of the incidence and open-label treatment of interferon-induced major depressive disorder in patients with hepatitis C. Mol Psychiatry. 2002; 7(9):942-7. DOI: 10.1038/sj.mp.4001119. View

16.

Leo R, Di Lorenzo G, Tesauro M, Razzini C, Forleo G, Chiricolo G . Association between enhanced soluble CD40 ligand and proinflammatory and prothrombotic states in major depressive disorder: pilot observations on the effects of selective serotonin reuptake inhibitor therapy. J Clin Psychiatry. 2007; 67(11):1760-6. DOI: 10.4088/jcp.v67n1114. View

17.

Mikova O, Yakimova R, Bosmans E, Kenis G, Maes M . Increased serum tumor necrosis factor alpha concentrations in major depression and multiple sclerosis. Eur Neuropsychopharmacol. 2001; 11(3):203-8. DOI: 10.1016/s0924-977x(01)00081-5. View

18.

Wichers M, Kenis G, Leue C, Koek G, Robaeys G, Maes M . Baseline immune activation as a risk factor for the onset of depression during interferon-alpha treatment. Biol Psychiatry. 2006; 60(1):77-9. DOI: 10.1016/j.biopsych.2005.11.024. View

19.

Anisman H, Kokkinidis L, Merali Z . Further evidence for the depressive effects of cytokines: anhedonia and neurochemical changes. Brain Behav Immun. 2002; 16(5):544-56. DOI: 10.1016/s0889-1591(02)00011-9. View

20.

Wood L, Nail L, Gilster A, Winters K, Elsea C . Cancer chemotherapy-related symptoms: evidence to suggest a role for proinflammatory cytokines. Oncol Nurs Forum. 2006; 33(3):535-42. DOI: 10.1188/06.ONF.535-542. View