Cellular Immunity to Varicella‐Zoster Virus in Patients with Major Depression

Irwin, Michael R.; Costlow, Carolyn; Williams, Heather; Artin, Kamal Haydari; Chan, Christina Y.; Stinson, Diane; Levin, Myron J.; Hayward, Anthony R.; Oxman, Michael N.

doi:10.1086/514272

Cited by 94 publications

(69 citation statements)

References 28 publications

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“…This is also in agreement with a number of early studies that suggest reduced cellular immune activity is associated with increased depression symptoms. 6,18,19 However, we did not find an interaction between CHF status and depression symptoms at rest, with further decreases in chemotaxis to SDF-1. This suggests that CHF status and depressive symptom levels are independently associated and likely additive for reductions in chemotaxis.…”

Section: Discussioncontrasting

confidence: 78%

A Potential Shift From Adaptive Immune Activity to Nonspecific Inflammatory Activation Associated With Higher Depression Symptoms in Chronic Heart Failure Patients

Redwine

Wirtz

Hong

et al. 2009

Journal of Cardiac Failure

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Background: Chronic heart failure (CHF) patients with elevated depression symptoms are at greater risk of morbidity and mortality. The mechanisms linking symptoms of depression with disease progression in CHF are unclear. However, research studies have found evidence of alterations in immune activity associated with depression symptoms that may influence heart function. The present study sought to determine the relationship between depression symptoms and chemotaxis of peripheral blood mononuclear cells (PBMCs) in CHF patients, both at rest and in response to moderate exercise. Methods and Results: Sixty-five patients diagnosed with CHF (mean age, 59.8 6 14.5 years) and 45 non-CHF control subjects (mean age, 52.1 6 11.6) completed the Beck Depression Inventory (BDI) before undergoing a moderate 20-minute bicycle exercise task. Chemotaxis of PBMCs was examined in vitro to a bacterial peptide f-met leu phe (fMLP) and a physiologic chemokine, stromal cell derived factor-1 (SDF-1) immediately before and after exercise. CHF patients had reduced chemotaxis to SDF-1 (P 5 .025) compared with non-CHF subjects. Higher BDI scores were associated with reduced baseline chemotaxis to SDF-1 in both CHF and non-CHF subjects (P 5 .027). In contrast, higher BDI scores were associated with increased chemotaxis to fMLP (P 5 .049) and SDF-1 (P 5 .018) in response to exercise in the CHF patients. Conclusion: The present study suggests a shift in immune cell mobility in CHF patients with greater depression symptom severity, with reduced chemotaxis to a physiologically specific chemokine at rest but increased chemotaxis to both nonspecific and specific chemical attractants in response to physical activity. This could have implications for cardiac repair and remodeling in CHF patients and therefore may affect disease progression.

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Section: Discussioncontrasting

confidence: 78%

A Potential Shift From Adaptive Immune Activity to Nonspecific Inflammatory Activation Associated With Higher Depression Symptoms in Chronic Heart Failure Patients

Redwine

Wirtz

Hong

et al. 2009

Journal of Cardiac Failure

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“…Depressed individuals also show patterns of immune alteration similar to those observed in chronic stress; e.g., impairments in some cellular immune parameters, delayed healing of experimentally administered wounds, and blunted antibody responses to vaccination, accompanied by increased systemic inflammatory activity (e.g., Bosch et al 2007;Glaser et al 2003;Irwin et al 1998;Kop et al 2002;Lesperance et al 2004;Miller et al 2002b; see reviews by Irwin 2001Irwin , 2002Raison et al 2006). Similar patterns are seen in both clinically depressed patients and those with high levels of dysphoric affect.…”

Section: Depressionmentioning

confidence: 78%

Health Psychology: Developing Biologically Plausible Models Linking the Social World and Physical Health

Miller

Chen

Cole

2009

Annu. Rev. Psychol.

515

436

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Research over the past several decades has documented psychosocial influences on the development and progression of several major medical illnesses. The field is now increasingly focused on identifying the biological and behavioral mechanisms underlying these effects. This review takes stock of the knowledge accumulated in the biological arena to date and highlights conceptual and methodological approaches that have proven especially productive. It emphasizes the value of a diseasecentered approach that "reverse engineers" adverse health outcomes into their specific biological determinants and then identifies psychologically modulated neuroendocrine and immunologic dynamics that modulate those pathological processes at the cellular and molecular levels.

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“…25 Major depressive disorder has also been shown to be associated with a marked decline in VZV-specific cellular immunity, compared to age-and sex-matched subjects with no history of depression. 22,25 There was a trend for the severity of depressive symptoms to be associated with lower ELISPOT counts, and the VZV responder cell frequency was higher in depressed patients treated with antidepressant medications compared to untreated depressed patients. 26 The mechanisms that account for the decline in VZV-specific cellular immunity in stressed and/or depressed patients are unknown.…”

Section: Discussionmentioning

confidence: 98%