Inflammation, sickness behaviour and depression

doi:10.1017/CBO9780511544293.013

12 - Inflammation, sickness behaviour and depression

from Part 3 - Biological and behavioural processes

Published online by Cambridge University Press: 17 September 2009

Maite Moreau and

Edited by

Robert Dantzer: Affiliation:
Integrative Neurobiology, Université Victor Segalen Bordeaux 2, Bordeaux, France
Nathalie Castanon: Affiliation:
Integrative Neurobiology, Université Victor Segalen Bordeaux 2, Bordeaux, France
Jacques Lestage: Affiliation:
Integrative Neurobiology, Université Victor Segalen Bordeaux 2, Bordeaux, France
Maite Moreau: Affiliation:
Integrative Neurobiology, Université Victor Segalen Bordeaux 2, Bordeaux, France
Lucile Capuron: Affiliation:
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA
Andrew Steptoe: Affiliation:
University College London

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Summary

Introduction

The prevalence of depression in medically ill patients is high, ranging from 5% to 20% versus 3–5% in the general population. The comorbidity of depressive disorders in general hospital patients or in-patients with chronic pathologies who consult general practitioners (GPs) is about 40% [1, 2]. The rates are similar in women with breast cancer [3]. Several studies have shown that patients with chronic diseases, including arthritis and coronary heart disease (CHD), are more at risk than healthy subjects for developing mood disorders [4–7]. In most of these studies, depression was identified as a significant risk factor for mortality and health/treatment complications. Depression was associated with greater physical limitation, more frequent subjective health complaints, lower treatment compliance and satisfaction, and reduced perceived quality of life. In addition, the prevalence of major depression in later life was also found to be more frequent among people with chronic illnesses [8].

Psychological factors are usually put forward to explain the comorbidity of depression with medical illnesses. Medically ill patients often suffer from physical limitations and have difficulties maintaining positive social relationships. They frequently report feelings of hopelessness, since they cannot cope with the problems they are confronted with, especially in situations of poor social support. These factors increase the risk for the occurrence of depressive disorders. Lack of compliance with medical treatments, decreased social support and the consequences of biological changes associated with depression (e.g. impaired cellular immune functions) are believed to account for the association between depression and increased morbidity and mortality.

Keywords

behavioural adjustments chronic medical pathologies depression inflammatory cytokines systemic inflammatory responses innate immune system innate immune cells

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Type: Chapter
Information: Depression and Physical Illness , pp. 265 - 279
DOI: https://doi.org/10.1017/CBO9780511544293.013 [Opens in a new window]
Publisher: Cambridge University Press
Print publication year: 2006

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References

Consoli, S. M., Depression and associated organic pathologies, a still under-estimated comorbidity: results of the DIALOGUE study. Presse Med. 32 (2003), 10–21.Google Scholar

Abidi, M. A., Gadit, A. A., Liaison psychiatry and referral rates among hospitalized patients. J. Coll. Physicians Surg. Pak. 13 (2003), 274–6.Google Scholar

Kissane, D. W., Grabsch, B., Love, A., et al., Psychiatric disorder in women with early stage and advanced breast cancer: a comparative analysis. Aust. N. Z. J. Psychiatry 38 (2004), 320–26.Google Scholar

Dunlop, D. D., Lyons, J. S., Manheim, L. M., Song, J., Chang, R. W., Arthritis and heart disease as risk factors for major depression: the role of functional limitation. Med. Care 42 (2004), 502–11.Google Scholar

Katz, P. P., Yelin, E. H., Prevalence and correlates of depressive symptoms among persons with rheumatoid arthritis. J. Rheumatol. 20 (1993), 790–96.Google Scholar

Murberg, T. A., Bru, E., Aarsland, T., Svebak, S., Functional status and depression among men and women with congestive heart failure. Int. J. Psychiatr. Med. 28 (1998), 273–91.Google Scholar

Spertus, J. A., McDonell, M., Woodman, C. L., Fihn, S. D., Association between depression and worse disease-specific functional status in outpatients with coronary artery disease. Am. Heart J. 140 (2000), 105–10.Google Scholar

Addington, A. M., Gallo, J. J., Ford, D. E., Eaton, W. W., Epidemiology of unexplained fatigue and major depression in the community: the Baltimore ECA follow-up, 1981–1994. Psychol. Med. 31 (2001), 1037–44.Google Scholar

Dantzer, R., Cytokine-induced sickness behaviour: where do we stand?Brain Behav. Immun. 15 (2001), 7–24.Google Scholar

Dantzer, R., Innate immunity at the forefront of psychoneuroimmunology. Brain Behav. Immun. 18 (2004), 1–6.Google Scholar

Beutler, B., Innate immunity: an overview. Mol. Immunol. 40 (2004), 845–59.Google Scholar

Kent, S., Bluthe, R. M., Dantzer, R., et al., Different receptor mechanisms mediate the pyrogenic and behavioural effects of interleukin 1. Proc. Natl. Acad. Sci. U. S. A. 89 (1992), 9117–20.Google Scholar

Parnet, P., Kelley, K. W., Bluthe, R. M., Dantzer, R., Expression and regulation of interleukin-1 receptors in the brain: role in cytokines-induced sickness behaviour. J. Neuroimmunol. 125 (2002), 5–14.Google Scholar

Dam, A. M., Brouns, M., Louisse, S., Berkenbosch, F., Appearance of interleukin-1 in macrophages and in ramified microglia in the brain of endotoxin-treated rats: a pathway for the induction of non-specific symptoms of sickness?Brain Res. 588 (1992), 291–6.Google Scholar

Laye, S., Parnet, P., Goujon, E., Dantzer, R., Peripheral administration of lipopolysaccharide induces the expression of cytokine transcripts in the brain and pituitary of mice. Brain Res. Mol. Brain Res. 27 (1994), 157–62.Google Scholar

Laye, S., Gheusi, G., Cremona, S., et al., Endogenous brain IL-1 mediates LPS-induced anorexia and hypothalamic cytokine expression. Am. J. Physiol. Regul. Integr. Comp. Physiol. 279 (2000), R93–8.Google Scholar

Dantzer, R., Konsman, J. P., Bluthe, R. M., Kelley, K. W., Neural and humoral pathways of communication from the immune system to the brain: parallel or convergent?Auton. Neurosci. 85 (2000), 60–65.Google Scholar

Luheshi, G. N., Bluthe, R. M., Rushforth, D., et al., Vagotomy attenuates the behavioural but not the pyrogenic effects of interleukin-1 in rats. Auton. Neurosci. 85 (2000), 127–32.Google Scholar

Konsman, J. P., Parnet, P., Dantzer, R., Cytokine-induced sickness behaviour: mechanisms and implications. Trends Neurosci. 25 (2002), 154–9.Google Scholar

Hart, B. L., Biological basis of the behaviour of sick animals. Neurosci. Biobehav. Rev. 12 (1988), 123–37.Google Scholar

Dantzer, R., Kelley, K. W., Stress and immunity: an integrated view of relationships between the brain and the immune system. Life Sci. 44 (1989), 1995–2008.Google Scholar

Kluger, M. J., Temperature regulation, fever, and disease. Int. Rev. Physiol. 20 (1979), 209–51.Google Scholar

Kluger, M. J., Is fever beneficial?Yale J. Biol. Med. 59 (1986), 89–95.Google Scholar

Watkins, L. R., Maier, S. F., The pain of being sick: implications of immune-to-brain communication for understanding pain. Annu. Rev. Psychol. 51 (2000), 29–57.Google Scholar

Miller, N. E., Some psychophysiological studies of motivation and of the behavioural effects of illness. Bull. Br. Psychol. Soc. 17 (1964), 1–20.Google Scholar

Aubert, A., Goodall, G., Dantzer, R., Compared effects of cold ambient temperature and cytokines on macronutrient intake in rats. Physiol. Behav. 57 (1995), 869–73.Google Scholar

Aubert, A., Vega, C., Dantzer, R., Goodall, G., Pyrogens specifically disrupt the acquisition of a task involving cognitive processing in the rat. Brain Behav. Immun. 9 (1995), 129–48.Google Scholar

Aubert, A., Goodall, G., Dantzer, R., Gheusi, G., Differential effects of lipopolysaccharide on pup retrieving and nest building in lactating mice. Brain Behav. Immun. 11 (1997), 107–18.Google Scholar

Anisman, H., Merali, Z., Cytokines, stress and depressive illness: brain–immune interactions. Ann. Med. 35 (2003), 2–11.Google Scholar

Capuron, L., Ravaud, A., Miller, A. H., Dantzer, R., Baseline mood and psychosocial characteristics of patients developing depressive symptoms during interleukin-2 and/or interferon-alpha cancer therapy. Brain Behav. Immun. 18 (2004), 205–13.Google Scholar

Capuron, L., Gumnick, J. F., Musselman, D. L., et al., Neurobehavioural effects of interferon-alpha in cancer patients: phenomenology and paroxetine responsiveness of symptom dimensions. Neuropsychopharmacology 26 (2002), 643–52.Google Scholar

Jones, I., Craddock, N., Candidate gene studies of bipolar disorder. Ann. Med. 33 (2001), 248–56.Google Scholar

Heim, C., Nemeroff, C. B., The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies. Biol. Psychiatry 49 (2001), 1023–39.Google Scholar

Capuron, L., Ravaud, A., Prediction of the depressive effects of interferon alfa therapy by the patient's initial affective state. N. Engl. J. Med. 340 (1999), 1370.Google Scholar

Miyaoka, H., Otsubo, T., Kamijima, K., et al., Depression from interferon therapy in patients with hepatitis C. Am. J. Psychiatry 156 (1999), 1120.Google Scholar

Capuron, L., Neurauter, G., Musselman, D. L., et al., Interferon-alpha-induced changes in tryptophan metabolism: relationship to depression and paroxetine treatment. Biol. Psychiatry 54 (2003), 906–14.Google Scholar

Constant, C., Castera, L., Dantzer, R., et al., Mood alterations during interferon-alpha therapy in chronic hepatitis C: evidence for an overlap between manic/hypomanic and depressive symptoms. J. Clin. Psychiatry 66 (2005), 1050–57.Google Scholar

Capuron, L., Ravaud, A., Neveu, P. J., et al., Association between decreased serum tryptophan concentrations and depressive symptoms in cancer patients undergoing cytokine therapy. Mol. Psychiatry 7 (2002), 468–73.Google Scholar

Maes, M., Bonaccorso, S., Marino, V., et al., Treatment with interferon-alpha (IFN alpha) of hepatitis C patients induces lower serum dipeptidyl peptidase IV activity, which is related to IFN alpha-induced depressive and anxiety symptoms and immune activation. Mol. Psychiatry 6 (2001), 475–80.Google Scholar

Lestage, J., Verrier, D., Palin, K., Dantzer, R., The enzyme indoleamine 2,3-dioxygenase is induced in the mouse brain in response to peripheral administration of lipopolysaccharide and superantigen. Brain Behav. Immun. 16 (2002), 596–601.Google Scholar

Juengling, F. D., Ebert, D., Gut, O., et al., Prefrontal cortical hypometabolism during low-dose interferon alpha treatment. Psychopharmacology (Berl.) 152 (2000), 383–9.Google Scholar

Capuron, L., Pagnoni, G., Lawson, D. H., et al., Altered fronto-pallidal activity during high-dose interferon-alpha treatment as determined by positron emission tomography. Abstr. Soc. Neurosci. (2002), 498.5.Google Scholar

Hashimoto, R., Nagatsu, T., Ohta, T., Mizutani, M., Omura, I., Changes in the concentrations of tetrahydrobiopterin, the cofactor of tyrosine hydroxylase, in blood under physical stress and in depression. Ann. N. Y. Acad. Sci. 1018 (2004), 378–86.Google Scholar

Gilchrist, M., Hesslinger, C., Befus, A. D., Tetrahydrobiopterin, a critical factor in the production and role of nitric oxide in mast cells. J. Biol. Chem. 278 (2003), 50 607–14.Google Scholar

Kitagami, T., Yamada, K., Miura, H., et al., Mechanism of systemically injected interferon-alpha impeding monoamine biosynthesis in rats: role of nitric oxide as a signal crossing the blood–brain barrier. Brain Res. 978 (2003), 104–14.Google Scholar

Appels, A., Bar, F. W., Bar, J., Bruggeman, C., Baets, M., Inflammation, depressive symptomtology, and coronary artery disease. Psychosom. Med. 62 (2000), 601–605.Google Scholar

Lesperance, F., Frasure-Smith, N., Theroux, P., Irwin, M., The association between major depression and levels of soluble intercellular adhesion molecule 1, interleukin-6, and C-reactive protein in patients with recent acute coronary syndromes. Am. J. Psychiatry 161 (2004), 271–7.Google Scholar

Cleeland, C. S., Bennett, G. J., Dantzer, R., et al., Are the symptoms of cancer and cancer treatment due to a shared biologic mechanism? A cytokine-immunologic model of cancer symptoms. Cancer 97 (2003), 2919–25.Google Scholar

Holmes, C., El-Okl, M., Williams, A. L., et al., Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer's disease. J. Neurol. Neurosurg. Psychiatry 74 (2003), 788–9.Google Scholar

Eikelenboom, P., Hoogendijk, W. J., Jonker, C., Tilburg, W., Immunological mechanisms and the spectrum of psychiatric syndromes in Alzheimer's disease. J. Psychiatr. Res. 36 (2002), 269–80.Google Scholar

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