Publication

Does tryptophan degradation along the kynurenine pathway mediate the association between pro-inflammatory immune activity and depressive symptoms?

Quak, J., Doornbos, B., Roest, A. M., Duivis, H. E., Vogelzangs, N., Nolen, W. A., Penninx, B. W. J. H., Kema, I. P. & de Jonge, P., Jul-2014, In : Psychoneuroendocrinology. 45, p. 202-210 9 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Quak, J., Doornbos, B., Roest, A. M., Duivis, H. E., Vogelzangs, N., Nolen, W. A., Penninx, B. W. J. H., Kema, I. P., & de Jonge, P. (2014). Does tryptophan degradation along the kynurenine pathway mediate the association between pro-inflammatory immune activity and depressive symptoms? Psychoneuroendocrinology, 45, 202-210. https://doi.org/10.1016/j.psyneuen.2014.03.013

Author

Quak, Jacqueline ; Doornbos, Bennard ; Roest, Annelieke M. ; Duivis, Hester E. ; Vogelzangs, Nicole ; Nolen, Willem A. ; Penninx, Brenda W. J. H. ; Kema, Ido P. ; de Jonge, Peter. / Does tryptophan degradation along the kynurenine pathway mediate the association between pro-inflammatory immune activity and depressive symptoms?. In: Psychoneuroendocrinology. 2014 ; Vol. 45. pp. 202-210.

Harvard

Quak, J, Doornbos, B, Roest, AM, Duivis, HE, Vogelzangs, N, Nolen, WA, Penninx, BWJH, Kema, IP & de Jonge, P 2014, 'Does tryptophan degradation along the kynurenine pathway mediate the association between pro-inflammatory immune activity and depressive symptoms?', Psychoneuroendocrinology, vol. 45, pp. 202-210. https://doi.org/10.1016/j.psyneuen.2014.03.013

Standard

Does tryptophan degradation along the kynurenine pathway mediate the association between pro-inflammatory immune activity and depressive symptoms? / Quak, Jacqueline; Doornbos, Bennard; Roest, Annelieke M.; Duivis, Hester E.; Vogelzangs, Nicole; Nolen, Willem A.; Penninx, Brenda W. J. H.; Kema, Ido P.; de Jonge, Peter.

In: Psychoneuroendocrinology, Vol. 45, 07.2014, p. 202-210.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Quak J, Doornbos B, Roest AM, Duivis HE, Vogelzangs N, Nolen WA et al. Does tryptophan degradation along the kynurenine pathway mediate the association between pro-inflammatory immune activity and depressive symptoms? Psychoneuroendocrinology. 2014 Jul;45:202-210. https://doi.org/10.1016/j.psyneuen.2014.03.013


BibTeX

@article{8a12ea66b1074b578fc37f5e4b8d1220,
title = "Does tryptophan degradation along the kynurenine pathway mediate the association between pro-inflammatory immune activity and depressive symptoms?",
abstract = "Background: Several studies have suggested that induced tryptophan (TRP) degradation through the kynurenine (KYN) pathway by the enzyme indoleamine 2,3-dioxygenase (IDO) is implicated in the relation between depression and inflammation. We investigated the role of tryptophan degradation in the relationship between inflammatory markers and depressive symptoms in the Netherlands Study of Depression and Anxiety (NESDA) and hypothesized that tryptophan degradation would mediate (part of) this association.Methods: 2812 Participants of NESDA were included in this study including 1042 persons with current major depressive disorder (MDD). Assessments of C-reactive protein (CRP), interleukin (IL)-6, tumor-necrosis factor (TNF)-alpha, KYN and TRP were obtained from fasting blood samples at the baseline assessment. Tryptophan degradation was estimated by calculating the ratio [KYN/TRP]. Depressive symptoms were measured with the Inventory of Depressive Symptomatology.Results: Significant associations between inflammation and depressive symptoms were found for CRP and IL-6, for the total group and the subgroup of patients with current MDD. Adjustment for KYN/TRP did not attenuate these associations. There were no significant indirect effects for CRP on depressive symptoms mediated by KYN/TRP for the whole group (B = -0.032; 95% CI: -0.103 to 0.028) and for the subgroup of patients with current MDD (B = 0.059; 95% CI: -0.037 to 0.165). Also IL-6 did not indirectly affect depressive symptoms through KYN/TRP in the total group (B = -0.023; 95% CI: -0.093 to 0.045) and in the MDD subgroup B = 0.052; 95% CI: -0.019 to 0.144). Finally, no significant relation between depressive symptoms and KYN/TRP was found in the whole group (beta = -0.019, p = 0.311) nor in the subgroup with MDD(beta = 0.025, p = 0.424).Conclusions: We did not find indications for tryptophan degradation, measured by KYN/TRP, to mediate the relationship between inflammation and depressive symptoms. (C) 2014 Elsevier Ltd. All rights reserved.",
keywords = "Indoleamine 2,3-dioxygenase, Depressive symptoms, Depression, Tryptophan, Kynurenine, Inflammation, INDOLEAMINE 2,3-DIOXYGENASE IDO, INTERFERON-ALPHA, MAJOR DEPRESSION, CALMETTE-GUERIN, ANXIETY NESDA, YOUNG FINNS, HEPATITIS-C, IFN-ALPHA, ACTIVATION, METABOLISM",
author = "Jacqueline Quak and Bennard Doornbos and Roest, {Annelieke M.} and Duivis, {Hester E.} and Nicole Vogelzangs and Nolen, {Willem A.} and Penninx, {Brenda W. J. H.} and Kema, {Ido P.} and {de Jonge}, Peter",
year = "2014",
month = jul,
doi = "10.1016/j.psyneuen.2014.03.013",
language = "English",
volume = "45",
pages = "202--210",
journal = "Psychoneuroendocrinology",
issn = "0306-4530",
publisher = "PERGAMON-ELSEVIER SCIENCE LTD",

}

RIS

TY - JOUR

T1 - Does tryptophan degradation along the kynurenine pathway mediate the association between pro-inflammatory immune activity and depressive symptoms?

AU - Quak, Jacqueline

AU - Doornbos, Bennard

AU - Roest, Annelieke M.

AU - Duivis, Hester E.

AU - Vogelzangs, Nicole

AU - Nolen, Willem A.

AU - Penninx, Brenda W. J. H.

AU - Kema, Ido P.

AU - de Jonge, Peter

PY - 2014/7

Y1 - 2014/7

N2 - Background: Several studies have suggested that induced tryptophan (TRP) degradation through the kynurenine (KYN) pathway by the enzyme indoleamine 2,3-dioxygenase (IDO) is implicated in the relation between depression and inflammation. We investigated the role of tryptophan degradation in the relationship between inflammatory markers and depressive symptoms in the Netherlands Study of Depression and Anxiety (NESDA) and hypothesized that tryptophan degradation would mediate (part of) this association.Methods: 2812 Participants of NESDA were included in this study including 1042 persons with current major depressive disorder (MDD). Assessments of C-reactive protein (CRP), interleukin (IL)-6, tumor-necrosis factor (TNF)-alpha, KYN and TRP were obtained from fasting blood samples at the baseline assessment. Tryptophan degradation was estimated by calculating the ratio [KYN/TRP]. Depressive symptoms were measured with the Inventory of Depressive Symptomatology.Results: Significant associations between inflammation and depressive symptoms were found for CRP and IL-6, for the total group and the subgroup of patients with current MDD. Adjustment for KYN/TRP did not attenuate these associations. There were no significant indirect effects for CRP on depressive symptoms mediated by KYN/TRP for the whole group (B = -0.032; 95% CI: -0.103 to 0.028) and for the subgroup of patients with current MDD (B = 0.059; 95% CI: -0.037 to 0.165). Also IL-6 did not indirectly affect depressive symptoms through KYN/TRP in the total group (B = -0.023; 95% CI: -0.093 to 0.045) and in the MDD subgroup B = 0.052; 95% CI: -0.019 to 0.144). Finally, no significant relation between depressive symptoms and KYN/TRP was found in the whole group (beta = -0.019, p = 0.311) nor in the subgroup with MDD(beta = 0.025, p = 0.424).Conclusions: We did not find indications for tryptophan degradation, measured by KYN/TRP, to mediate the relationship between inflammation and depressive symptoms. (C) 2014 Elsevier Ltd. All rights reserved.

AB - Background: Several studies have suggested that induced tryptophan (TRP) degradation through the kynurenine (KYN) pathway by the enzyme indoleamine 2,3-dioxygenase (IDO) is implicated in the relation between depression and inflammation. We investigated the role of tryptophan degradation in the relationship between inflammatory markers and depressive symptoms in the Netherlands Study of Depression and Anxiety (NESDA) and hypothesized that tryptophan degradation would mediate (part of) this association.Methods: 2812 Participants of NESDA were included in this study including 1042 persons with current major depressive disorder (MDD). Assessments of C-reactive protein (CRP), interleukin (IL)-6, tumor-necrosis factor (TNF)-alpha, KYN and TRP were obtained from fasting blood samples at the baseline assessment. Tryptophan degradation was estimated by calculating the ratio [KYN/TRP]. Depressive symptoms were measured with the Inventory of Depressive Symptomatology.Results: Significant associations between inflammation and depressive symptoms were found for CRP and IL-6, for the total group and the subgroup of patients with current MDD. Adjustment for KYN/TRP did not attenuate these associations. There were no significant indirect effects for CRP on depressive symptoms mediated by KYN/TRP for the whole group (B = -0.032; 95% CI: -0.103 to 0.028) and for the subgroup of patients with current MDD (B = 0.059; 95% CI: -0.037 to 0.165). Also IL-6 did not indirectly affect depressive symptoms through KYN/TRP in the total group (B = -0.023; 95% CI: -0.093 to 0.045) and in the MDD subgroup B = 0.052; 95% CI: -0.019 to 0.144). Finally, no significant relation between depressive symptoms and KYN/TRP was found in the whole group (beta = -0.019, p = 0.311) nor in the subgroup with MDD(beta = 0.025, p = 0.424).Conclusions: We did not find indications for tryptophan degradation, measured by KYN/TRP, to mediate the relationship between inflammation and depressive symptoms. (C) 2014 Elsevier Ltd. All rights reserved.

KW - Indoleamine 2,3-dioxygenase

KW - Depressive symptoms

KW - Depression

KW - Tryptophan

KW - Kynurenine

KW - Inflammation

KW - INDOLEAMINE 2,3-DIOXYGENASE IDO

KW - INTERFERON-ALPHA

KW - MAJOR DEPRESSION

KW - CALMETTE-GUERIN

KW - ANXIETY NESDA

KW - YOUNG FINNS

KW - HEPATITIS-C

KW - IFN-ALPHA

KW - ACTIVATION

KW - METABOLISM

U2 - 10.1016/j.psyneuen.2014.03.013

DO - 10.1016/j.psyneuen.2014.03.013

M3 - Article

VL - 45

SP - 202

EP - 210

JO - Psychoneuroendocrinology

JF - Psychoneuroendocrinology

SN - 0306-4530

ER -

ID: 13455957