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Cytokines in depression and heart failure
Jagoda Pasic1, Wayne C Levy, Mark D Sullivan
1Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington, USA. jpasic@u.washington.edu
Insights
Cytokines may link depression and heart failure, impacting brain-body interactions. Further research into these immunological mechanisms is needed to understand the comorbidity of congestive heart failure (CHF) and major depression.
Area of Science:
- Immunology
- Cardiology
- Psychiatry
Background:
- Depression is linked to cardiovascular disease and mortality.
- Depression is a risk factor for congestive heart failure (CHF), with higher mortality and hospitalizations in affected patients.
- Neurobiological or neuroimmune mechanisms for heart failure and depression comorbidity are not yet established.
Purpose of the Study:
- Review the role of cytokines in CHF and depression as separate conditions.
- Identify overlapping immunological mechanisms in comorbid depression and CHF.
- Explore potential future research avenues for the pathophysiology of comorbid depression and CHF.
Main Methods:
- Literature review focusing on recent studies.
- Analysis of immunological mechanisms in CHF and depression.
- Identification of cytokine involvement in the comorbidity.
Main Results:
- Cytokines can have detrimental effects on the heart.
- Major depression is associated with alterations in the innate immune system, including cytokines.
- The immunoregulatory effects of antidepressants remain inconclusive.
Conclusions:
- The role of cytokines in comorbid depression and CHF is not yet fully understood.
- Cytokines may offer a novel pathway for understanding brain-body interactions in depression and heart failure.
- Further research is warranted to elucidate the immunological underpinnings of this comorbidity.
Objective:
There is a convincing body of evidence linking depression, cardiovascular disease, and mortality. There is also growing evidence that depression is a risk factor for congestive heart failure (CHF) and that CHF patients with major depression have higher rates of mortality and repeat hospitalizations. Currently there are no proposed neurobiological or neuroimmune mechanisms for the comorbidity of heart failure and depression.
Methods:
This review focuses on the recent literature about the role of cytokines in CHF and depression as separate conditions. This review also attempts to identify the overlapping immunological mechanisms that have a potential for future research in the pathophysiology of comorbid depression and CHF.
Results:
Results of current studies suggest that cytokines exert deleterious effects on the heart and that soluble tumor necrosis factor (TNF) receptor 2 leads to reversal of the cardiotoxic effects of TNF, although the clinical significance of this is unclear. Major depression has been associated with alteration of various aspects of the innate immune system, including cellular components (such as microphages, neutrophils, and natural killer cells) and soluble mediators (such as acute-phase reaction proteins and cytokines). It is inconclusive whether antidepressants have immunoregulatory effects.
Conclusions:
The literature has not yet addressed the role of cytokines in comorbid depression and CHF. But cytokines may provide a new avenue in understanding brain-body interaction in depression and heart failure.