Sickness behavior

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File:Michael Ancher 001.jpg
Ancher, Michael, "The Sick Girl", 1882, Statens Museum for Kunst

Sickness behavior is a coordinated set of adaptive behavioral changes that develop in ill individuals during the course of an infection. [1] They usually (but not necessarily)[2] accompany fever and aid survival. Such illness responses include lethargy, depression, anxiety, loss of appetite,[3][4] sleepiness,[5] hyperalgesia[6], reduction in grooming[1][7] and failure to concentrate.[8] Sickness behavior is a motivational state that reorganizes the organism's priorities to cope with infectious pathogens.[9][10] It has been suggested as relevant to understanding depression, and some aspects of the suffering that occurs in cancer.

History

Sick animals have long been recognized by farmers as having different behavior. Initially it was thought that this was due to physical weakness that resulted from diverting energy to the body processes needed to fight infection. However, in the 1960s, it was shown that animals produced a blood-carried ‘‘factor X’’ that acted upon the brain to cause sickness behavior.[11][12] In 1987, Benjamin L. Hart brought together a variety of research findings that argued for them being survival adaptations that if prevented would disadvantage an animal’s ability to fight infection. In the 1980s, the blood borne factor was shown to be proinflammatory cytokines produced by activated leukocytes in the immune system in response to lipopolysaccharides (a cell wall component of Gram-negative bacteria). These cytokines acted by various humoral and nerve routes upon the hypothalamus and other areas of the brain. Further research showed that the brain can also learn to control the various components of sickness behavior independently of immune activation.

General advantage

Sickness behavior in its different aspects causes an animal to limit its movement and so reduce its energy expenditure allowing this to be diverted to mobilize the fever response which involves raising body temperature.[1] This also limits an animal’s exposure to predators while it is cognitively and physically impaired.[1]

Specific advantages

The individual components of sickness behavior have specific individual advantages. Anorexia limits food ingestion and therefore reduces the availability of iron in the gut (and from gut absorption). Iron may aid bacterial reproduction so their reduction is useful during sickness.[13] Plasma concentrations of iron are lowered for this anti-bacterial reason in fever.[14] Lowered threshold for pain ensures that an animal is attentive that it does not place pressure on injured and inflamed tissues that might disrupt their healing.[1] Reduced grooming is adaptive since it reduces water loss.[1]

Immune control

Lipopolysaccharides trigger the immune system to produce proinflammatory cytokines IL-1, IL-6, and tumor necrosis factor (TNF).[15] These peripherally released cytokines act on the brain via a fast transmission pathway involving primary input through the vagus nerves,[16][17] and a slow transmission pathway involving cytokines originating from the choroid plexus and circumventricular organs and diffusing into the brain parenchyma by volume transmission.[18] Peripheral cytokines may enter the brain directly.[19][20] They may also induce the expression of other cytokines in the brain that cause sickness behavior.[21][22] Acute psychosocial stress enhances the ability of an immune response to trigger both inflammation and behavioral sickness.[23]

Behavioral conditioning

The components of sickness behavior can be learned by conditional association. For example, if a saccharin solution is given with a chemical that triggers a particular aspect of sickness behavior, on later occasions the saccharin solution will trigger it by itself.[24][25]

Depression

It has been proposed that major depressive disorder is near-identical with sickness behavior, so raising the possibility that it is a maladaptive manifestation of sickness behavior due to abnormalities in circulating cytokines.[26][27][28] The moods effects caused by interleukin-6 following an immune response has been linked to increased activity within the subgenual anterior cingulate cortex[29], an area involved in the etiology of depression.[30] Inflammation-associated mood change can also produce a reduction in the functional connectivity of this part of the brain to the amygdala, medial prefrontal cortex, nucleus accumbens, and superior temporal sulcus.[29]

Cancer side effect

In cancer, both the disease and the chemotherapy treatment can cause proinflammatory cytokine release which can cause sickness behavior as a side effect.[31][32]

See also

References

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  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Hart, B. L. (1988) "Biological basis of the behavior of sick animals". Neurosci Biobehav Rev. 12: 123-137. PubMed
  2. ↑ Kent, S., Bluthe, R. M., Dantzer, R., Hardwick, A. J., Kelley, K. W., Rothwell, N. J. Vannice, J. L. (1992) "Different receptor mechanisms mediate the pyrogenic and behavioral effects of interleukin 1". Proc Natl Acad Sci U S A. 89: 9117-9120. PubMed
  3. ↑ Exton, M. S. (1997) "Infection-induced anorexia: active host defence strategy". Appetite. 29: 369-383. PubMed
  4. ↑ Murray, M. J. Murray, A. B. (1979) "Anorexia of infection as a mechanism of host defense". Am J Clin Nutr. 32: 593-596. PubMed
  5. ↑ Mullington, J., Korth, C., Hermann, D. M., Orth, A., Galanos, C., Holsboer, F. Pollmacher, T. (2000) "Dose-dependent effects of endotoxin on human sleep". Am J Physiol Regul Integr Comp Physiol. 278: R947-955 PubMed
  6. ↑ Maier, S. F., Wiertelak, E. P., Martin, D. Watkins, L. R. (1993) "Interleukin-1 mediates the behavioral hyperalgesia produced by lithium chloride and endotoxin". Brain Res. 623: 321-324. PubMed
  7. ↑ Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  8. ↑ Kelley, K. W., Bluthe, R. M., Dantzer, R., Zhou, J. H., Shen, W. H., Johnson, R. W. Broussard, S. R. (2003) "Cytokine-induced sickness behavior". Brain Behav Immun. 17 Suppl 1: S112-118. PubMed
  9. ↑ Johnson, R. (2002) "The concept of sickness behavior: a brief chronological account of four key discoveries". Veterinary Immunology and Immunopathology. 87: 443-450 PubMed
  10. ↑ Kelley, K. W., Bluthe, R. M., Dantzer, R., Zhou, J. H., Shen, W. H., Johnson, R. W. Broussard, S. R. (2003) "Cytokine-induced sickness behavior". Brain Behav Immun. 17 Suppl 1: S112-118 PubMed
  11. ↑ Holmes, J. E. Miller, N. E. (1963) "Effects of Bacterial Endotoxin on Water Intake, Food Intake, and Body Temperature in the Albino Rat". J Exp Med. 118: 649-658 PubMed
  12. ↑ Miller, N. (1964) "Some psychophysiological studies of motivation and of the behavioral effects of illness". Bull. Br. Psychol. Soc. 17: 1-20
  13. ↑ Kluger, M. J. Rothenburg, B. A. (1979) "Fever and reduced iron: their interaction as a host defense response to bacterial infection". Science. 203: 374-376. PubMed
  14. ↑ Weinberg, E. D. (1984) "Iron withholding: a defense against infection and neoplasia". Physiol Rev. 64: 65-102. PubMed
  15. ↑ Kent, S., Bluthe, R. M., Dantzer, R., Hardwick, A. J., Kelley, K. W., Rothwell, N. J. Vannice, J. L. (1992) "Different receptor mechanisms mediate the pyrogenic and behavioral effects of interleukin 1". Proc Natl Acad Sci U S A. 89: 9117-9120 PubMed
  16. ↑ Goehler, L. E., Gaykema, R. P., Nguyen, K. T., Lee, J. E., Tilders, F. J., Maier, S. F. Watkins, L. R. (1999) "Interleukin-1beta in immune cells of the abdominal vagus nerve: a link between the immune and nervous systems?" J Neurosci. 19: 2799-2806 PubMed
  17. ↑ Goehler, L. E., Relton, J. K., Dripps, D., Kiechle, R., Tartaglia, N., Maier, S. F. Watkins, L. R. (1997) "Vagal paraganglia bind biotinylated interleukin-1 receptor antagonist: a possible mechanism for immune-to-brain communication". Brain Res Bull. 43: 357-364 PubMed
  18. ↑ Konsman, J. P., Kelley, K. Dantzer, R. (1999) "Temporal and spatial relationships between lipopolysaccharide-induced expression of Fos, interleukin-1beta and inducible nitric oxide synthase in rat brain". Neuroscience. 89: 535-548 PubMed
  19. ↑ Banks, W. A., Kastin, A. J. Gutierrez, E. G. (1994) "Penetration of interleukin-6 across the murine blood-brain barrier". Neurosci Lett. 179: 53-56 PubMed
  20. ↑ Banks, W. A., Ortiz, L., Plotkin, S. R. Kastin, A. J. (1991) "Human interleukin (IL) 1 alpha, murine IL-1 alpha and murine IL-1 beta are transported from blood to brain in the mouse by a shared saturable mechanism". J Pharmacol Exp Ther. 259: 988-996 PubMed
  21. ↑ Ban, E., Haour, F. Lenstra, R. (1992) "Brain interleukin 1 gene expression induced by peripheral lipopolysaccharide administration". Cytokine. 4: 48-54 PubMed
  22. ↑ van Dam, A. M., Brouns, M., Louisse, S. Berkenbosch, F. (1992) "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: 291-296 PubMed
  23. ↑ Brydon L, Walker C, Wawrzyniak A, Whitehead D, Okamura H, Yajima J, Tsuda A, Steptoe A. (2009). Synergistic effects of psychological and immune stressors on inflammatory cytokine and sickness responses in humans. Brain Behav Immun. 23(2):217-24. PMID 18835437 doi:10.1016/j.bbi.2008.09.007
  24. ↑ Exton, M. S., Bull, D. F. King, M. G. (1995) "Behavioral conditioning of lipopolysaccharide-induced anorexia". Physiol Behav. 57: 401-405. PubMed
  25. ↑ Exton, M. S., Bull, D. F., King, M. G. Husband, A. J. (1995) "Modification of body temperature and sleep state using behavioral conditioning". Physiol Behav. 57: 723-729. PubMed
  26. ↑ Charlton, B. G. (2000) "The malaise theory of depression: major depressive disorder is sickness behavior and antidepressants are analgesic". Med Hypotheses. 54: 126-130 PubMed
  27. ↑ Dantzer, R., O'Connor, J. C., Freund, G. G., Johnson, R. W. Kelley, K. W. (2008) "From inflammation to sickness and depression: when the immune system subjugates the brain". Nat Rev Neurosci. 9: 46-56 PubMed
  28. ↑ Maes, M. (2008) "The cytokine hypothesis of depression: inflammation, oxidative & nitrosative stress (IO&NS) and leaky gut as new targets for adjunctive treatments in depression". Neuro Endocrinol Lett. 29: 287-291 PubMed
  29. ↑ 29.0 29.1 Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  30. ↑ Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found. PDF:http://mbldownloads.com/0808CNS_BrainRegions.pdf
  31. ↑ Cleeland, C. S., Bennett, G. J., Dantzer, R., Dougherty, P. M., Dunn, A. J., Meyers, C. A., Miller, A. H., Payne, R., Reuben, J. M., Wang, X. S. Lee, B. N. (2003) "Are the symptoms of cancer and cancer treatment due to a shared biologic mechanism? A cytokine-immunologic model of cancer symptoms". Cancer. 97: 2919-2925 PubMed
  32. ↑ Myers, J. S. (2008) "Proinflammatory cytokines and sickness behavior: implications for depression and cancer-related symptoms". Oncol Nurs Forum. 35: 802-807 PubMed
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