Letters to the Editor
Proinflammatory Cytokines:
A Common Denominator in Depression and Somatic Symptoms?
Dear Editor:
Over the last decade, psychoneuroimmunological studies have reported the presence of immune disturbances in several psychiatric disorders and confirmed the effects of proinflammatory cytokines on neurobehavioural processes (1). Reported successes with antidepressant use in treating the somatic symptoms of functional somatic syndromes may point to a shared causal, but hitherto unknown, factor between these disorders and depression (2). We argue that abnormal proinflammatory cytokine production may be a shared causal factor. Our hypothesis rests on 3 facts. First, cytokines can influence cerebral function and cytokine receptors have been shown on many cerebral structures (3). Microglial cells and astrocytes can produce cytokines (4). Among the cytokines with effects that could have a bearing on psychopathology are the proinflammatory cytokines IL-1, IL-2, IL-6, and TNF (1). Second, abnormal proinflammatory cytokine activity has been implicated in major depression and reported in some functional somatic syndromes (5,6). Third, antidepressants that are used successfully in treating depression, and for which partial success has been reported with regard to the somatic symptoms of functional somatic syndromes, have antiinflammatory properties. Antidepressants have, in fact, been shown to have immunomodulatory effects (7), and all antidepressant drugs, irrespective of their pharmacologic class, are able to attenuate the behavioural and neuroendocrine effects of immune activation (8). We therefore conclude that proinflammatory cytokine production may be a shared causal factor in depression and functional somatic syndromes and that the antiinflammatory properties of antidepressants may account for their reported success in the treatment of these disorders.
References
1. Muller M, Ackenheil M. Psychoneuroimunology and the cytokine action in the CNS: implication for psychiatric disorders. Prog Neuropsychopharmacol Biol 1998;22:1–33.
2. Stahl SM. Antidepressants and somatic symptoms: therapeutic actions are expanding beyond affective spectrum disorders to functional somatic syndromes. J Clin Psychiatry 2003;64:745–6.
3. Haas HS, Schauenstein KS. Neuroimmunomodulation via the limbic structures—the neuroanatomy of psychoimmunology. Prog Neurobiol 1997;51:195–222.
4. Fabry Z, Raine CS, Hart MN. Nervous tissue as an immune compartment: the dialect of the immune response in the CNS. Immunol Today 1994;15:218–24.
5. Maes M. Major depression and activation of the inflammatory response system. In: Dantzer R, Wollman EE, Yirmiya R, editors. Cytokines, stress and depression, advances in experimental medicine and biology. Volume 461. New York: Kluwer Academic/Plenum Publishers; 1999. p 25–46.
6. Visser JTJ, De Kloet ER, Nagelkerken L. Altered glucocorticoid regulation of the immune response in chronic fatigue syndrome. Ann NY Acad Sci 2000;917:868–75.
7. Szelenyi J, Selmeczy Z. Immunomodulatory effect of antidepressants. Curr Opin Pharmacol 2002:2;428–43.
8. Capuron L, Dantzer R. Cytokines and depression: the need for a new paradigm. Brain Behav Immun 2003;17(Suppl 1: S119–S124.)
Margaretha Viljoen, PhD, PhD
Annie Panzer, MBChB, PhD
Pretoria, South Africa
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