Cytokine genes TNF, IL1A, IL1B, IL6, IL1RN and IL10, and childhood-onset mood disorders

V. L. Misener, L. Gomez, K. G. Wigg, P. Luca, N. King, E. Kiss, G. Daróczi, K. Kapornai, Z. Tamas, L. Mayer, J. Gádoros, I. Baji, J. L. Kennedy, M. Kovacs, A. Vetró, C. L. Barr, István Benák, Viola Kothencné Osváth, Edit Dombovári, Emília Kaczvinszky & 6 others László Mayer, Júlia Gádoros, Ildikó Baji, Z. Tamás, Márta Besnyo, Judit Székely

Research output: Contribution to journalArticle

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Abstract

Background/Aims: Inflammatory cytokines induce a behavioral syndrome, known as sickness behavior, that strongly resembles symptoms typically seen in depression. This resemblance has led to the theory that an imbalance of inflammatory cytokine activity may be a contributing factor in depressive disorders. Support for this is found in multiple lines of evidence, such as the effects of cytokines on the activities of the hypothalamic-pituitary-adrenal axis, serotonin and brain-derived neurotrophic factor, and hippocampal function, all of which are implicated in the etiology of depression. In addition, associations between inflammatory activity and depressive symptomology have been documented in a number of studies, and the depressogenic effects of cytokine therapy are well known. Accordingly, given that depression has a substantial genetic basis, genes involved in the regulation of inflammatory cytokine activity are strong candidates for involvement in genetic susceptibility to depressive disorders. Here, we have tested 6 key genes of this type, TNF, IL1A, IL1B, IL6, IL1RN and IL10, as candidates for involvement in childhood-onset mood disorders. Methods: In this study of 384 families, each ascertained through a child with depression diagnosed before the age of 15 years, 11 polymorphisms of known or likely functional significance (coding and regulatory variants) were analyzed. Results: Testing for biased transmission of alleles from parents to their affected offspring, we found no evidence for an association between childhood-onset mood disorders and any of the polymorphisms, either individually or as haplotypes. Conclusion: The present study does not support the involvement of the TNF, IL1A, IL1B, IL6, IL1RN and IL10 variants as major genetic risk factors contributing to early-onset mood disorders.

Original languageEnglish
Pages (from-to)71-80
Number of pages10
JournalNeuropsychobiology
Volume58
Issue number2
DOIs
Publication statusPublished - Oct 2008

Fingerprint

Mood Disorders
Interleukin-10
Interleukin-6
Cytokines
Depression
Genes
Depressive Disorder
Illness Behavior
Brain-Derived Neurotrophic Factor
Genetic Predisposition to Disease
Haplotypes
Serotonin
Parents
Alleles
Therapeutics

Keywords

  • Depression, childhood
  • Inflammatory cytokines
  • Mood disorders, genetic associations

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Neuropsychology and Physiological Psychology
  • Biological Psychiatry

Cite this

Misener, V. L., Gomez, L., Wigg, K. G., Luca, P., King, N., Kiss, E., ... Székely, J. (2008). Cytokine genes TNF, IL1A, IL1B, IL6, IL1RN and IL10, and childhood-onset mood disorders. Neuropsychobiology, 58(2), 71-80. https://doi.org/10.1159/000159775

Cytokine genes TNF, IL1A, IL1B, IL6, IL1RN and IL10, and childhood-onset mood disorders. / Misener, V. L.; Gomez, L.; Wigg, K. G.; Luca, P.; King, N.; Kiss, E.; Daróczi, G.; Kapornai, K.; Tamas, Z.; Mayer, L.; Gádoros, J.; Baji, I.; Kennedy, J. L.; Kovacs, M.; Vetró, A.; Barr, C. L.; Benák, István; Osváth, Viola Kothencné; Dombovári, Edit; Kaczvinszky, Emília; Mayer, László; Gádoros, Júlia; Baji, Ildikó; Tamás, Z.; Besnyo, Márta; Székely, Judit.

In: Neuropsychobiology, Vol. 58, No. 2, 10.2008, p. 71-80.

Research output: Contribution to journalArticle

Misener, VL, Gomez, L, Wigg, KG, Luca, P, King, N, Kiss, E, Daróczi, G, Kapornai, K, Tamas, Z, Mayer, L, Gádoros, J, Baji, I, Kennedy, JL, Kovacs, M, Vetró, A, Barr, CL, Benák, I, Osváth, VK, Dombovári, E, Kaczvinszky, E, Mayer, L, Gádoros, J, Baji, I, Tamás, Z, Besnyo, M & Székely, J 2008, 'Cytokine genes TNF, IL1A, IL1B, IL6, IL1RN and IL10, and childhood-onset mood disorders', Neuropsychobiology, vol. 58, no. 2, pp. 71-80. https://doi.org/10.1159/000159775
Misener, V. L. ; Gomez, L. ; Wigg, K. G. ; Luca, P. ; King, N. ; Kiss, E. ; Daróczi, G. ; Kapornai, K. ; Tamas, Z. ; Mayer, L. ; Gádoros, J. ; Baji, I. ; Kennedy, J. L. ; Kovacs, M. ; Vetró, A. ; Barr, C. L. ; Benák, István ; Osváth, Viola Kothencné ; Dombovári, Edit ; Kaczvinszky, Emília ; Mayer, László ; Gádoros, Júlia ; Baji, Ildikó ; Tamás, Z. ; Besnyo, Márta ; Székely, Judit. / Cytokine genes TNF, IL1A, IL1B, IL6, IL1RN and IL10, and childhood-onset mood disorders. In: Neuropsychobiology. 2008 ; Vol. 58, No. 2. pp. 71-80.
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AU - Misener, V. L.

AU - Gomez, L.

AU - Wigg, K. G.

AU - Luca, P.

AU - King, N.

AU - Kiss, E.

AU - Daróczi, G.

AU - Kapornai, K.

AU - Tamas, Z.

AU - Mayer, L.

AU - Gádoros, J.

AU - Baji, I.

AU - Kennedy, J. L.

AU - Kovacs, M.

AU - Vetró, A.

AU - Barr, C. L.

AU - Benák, István

AU - Osváth, Viola Kothencné

AU - Dombovári, Edit

AU - Kaczvinszky, Emília

AU - Mayer, László

AU - Gádoros, Júlia

AU - Baji, Ildikó

AU - Tamás, Z.

AU - Besnyo, Márta

AU - Székely, Judit

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N2 - Background/Aims: Inflammatory cytokines induce a behavioral syndrome, known as sickness behavior, that strongly resembles symptoms typically seen in depression. This resemblance has led to the theory that an imbalance of inflammatory cytokine activity may be a contributing factor in depressive disorders. Support for this is found in multiple lines of evidence, such as the effects of cytokines on the activities of the hypothalamic-pituitary-adrenal axis, serotonin and brain-derived neurotrophic factor, and hippocampal function, all of which are implicated in the etiology of depression. In addition, associations between inflammatory activity and depressive symptomology have been documented in a number of studies, and the depressogenic effects of cytokine therapy are well known. Accordingly, given that depression has a substantial genetic basis, genes involved in the regulation of inflammatory cytokine activity are strong candidates for involvement in genetic susceptibility to depressive disorders. Here, we have tested 6 key genes of this type, TNF, IL1A, IL1B, IL6, IL1RN and IL10, as candidates for involvement in childhood-onset mood disorders. Methods: In this study of 384 families, each ascertained through a child with depression diagnosed before the age of 15 years, 11 polymorphisms of known or likely functional significance (coding and regulatory variants) were analyzed. Results: Testing for biased transmission of alleles from parents to their affected offspring, we found no evidence for an association between childhood-onset mood disorders and any of the polymorphisms, either individually or as haplotypes. Conclusion: The present study does not support the involvement of the TNF, IL1A, IL1B, IL6, IL1RN and IL10 variants as major genetic risk factors contributing to early-onset mood disorders.

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KW - Inflammatory cytokines

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