The catecholamine-cytokine balance: Interaction between the brain and the immune system

Research output: Conference contribution

84 Citations (Scopus)

Abstract

Cytokines are involved both in various immune reactions and in controlling certain events in the central nervous system (CNS). In our earlier studies, it was shown that monoamine neurotransmitters, released in stress situations, represent a tonic sympathetic control on cytokine production and on the balance of proinflammatory/anti-inflammatory cytokines. Basic and clinical studies have provided evidence that the biophase level of monoamines, determined by the balance of their release and uptake, is involved in the pathophysiology and treatment of depression, while inflammatory mediators might also have a role in its etiology. In this work, we studied the role of changes in norepinephrine (NE) level on the lipopolysaccharide (LPS) evoked tumor necrosis factor (TNF)-α and interleukin (IL)-10 response both in the plasma and in the hippocampus of mice. We demonstrated that the LPS induced TNF-α response is in direct correlation with the biophase level of NE, as it is significantly higher when the release of NE of vesicular origin was completely inhibited in an animal model of depression (reserpine treatment) and it is significantly lower in the case of increasing biophase levels of NE by genetic (NET-KO) or chemical (desipramine) disruption of NE reuptake. IL-10 was changed inversely to TNF-α levels only in the desipramine-treated animals. Our results showed that depression is related both to changes in peripheral and in hippocampal inflammatory cytokine production and to monoamine neurotransmitter levels. Since several anti-inflammatory drugs also have antidepressant effects, we hypothesized that antidepressants are also able to modulate the LPS-induced inflammatory response, which might contribute to their antidepressant effect.

Original languageEnglish
Title of host publicationAnnals of the New York Academy of Sciences
Pages311-324
Number of pages14
Volume1113
DOIs
Publication statusPublished - okt. 2007

Publication series

NameAnnals of the New York Academy of Sciences
Volume1113
ISSN (Print)00778923
ISSN (Electronic)17496632

Fingerprint

Immune system
Catecholamines
Immune System
Brain
Norepinephrine
Cytokines
Antidepressive Agents
Lipopolysaccharides
Desipramine
Tumor Necrosis Factor-alpha
Interleukin-10
Neurotransmitter Agents
Animals
Anti-Inflammatory Agents
Antigen-antibody reactions
Reserpine
Neurology
Hippocampus
Central Nervous System
Animal Models

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Szelényi, J., & Vízi, E. (2007). The catecholamine-cytokine balance: Interaction between the brain and the immune system. In Annals of the New York Academy of Sciences (Vol. 1113, pp. 311-324). (Annals of the New York Academy of Sciences; Vol. 1113). https://doi.org/10.1196/annals.1391.026

The catecholamine-cytokine balance : Interaction between the brain and the immune system. / Szelényi, J.; Vízi, E.

Annals of the New York Academy of Sciences. Vol. 1113 2007. p. 311-324 (Annals of the New York Academy of Sciences; Vol. 1113).

Research output: Conference contribution

Szelényi, J & Vízi, E 2007, The catecholamine-cytokine balance: Interaction between the brain and the immune system. in Annals of the New York Academy of Sciences. vol. 1113, Annals of the New York Academy of Sciences, vol. 1113, pp. 311-324. https://doi.org/10.1196/annals.1391.026
Szelényi J, Vízi E. The catecholamine-cytokine balance: Interaction between the brain and the immune system. In Annals of the New York Academy of Sciences. Vol. 1113. 2007. p. 311-324. (Annals of the New York Academy of Sciences). https://doi.org/10.1196/annals.1391.026
Szelényi, J. ; Vízi, E. / The catecholamine-cytokine balance : Interaction between the brain and the immune system. Annals of the New York Academy of Sciences. Vol. 1113 2007. pp. 311-324 (Annals of the New York Academy of Sciences).
@inproceedings{2c68f91dad504acabdea80e93f4c2559,
title = "The catecholamine-cytokine balance: Interaction between the brain and the immune system",
abstract = "Cytokines are involved both in various immune reactions and in controlling certain events in the central nervous system (CNS). In our earlier studies, it was shown that monoamine neurotransmitters, released in stress situations, represent a tonic sympathetic control on cytokine production and on the balance of proinflammatory/anti-inflammatory cytokines. Basic and clinical studies have provided evidence that the biophase level of monoamines, determined by the balance of their release and uptake, is involved in the pathophysiology and treatment of depression, while inflammatory mediators might also have a role in its etiology. In this work, we studied the role of changes in norepinephrine (NE) level on the lipopolysaccharide (LPS) evoked tumor necrosis factor (TNF)-α and interleukin (IL)-10 response both in the plasma and in the hippocampus of mice. We demonstrated that the LPS induced TNF-α response is in direct correlation with the biophase level of NE, as it is significantly higher when the release of NE of vesicular origin was completely inhibited in an animal model of depression (reserpine treatment) and it is significantly lower in the case of increasing biophase levels of NE by genetic (NET-KO) or chemical (desipramine) disruption of NE reuptake. IL-10 was changed inversely to TNF-α levels only in the desipramine-treated animals. Our results showed that depression is related both to changes in peripheral and in hippocampal inflammatory cytokine production and to monoamine neurotransmitter levels. Since several anti-inflammatory drugs also have antidepressant effects, we hypothesized that antidepressants are also able to modulate the LPS-induced inflammatory response, which might contribute to their antidepressant effect.",
keywords = "Catecholamine, Cytokine, Depression, Inflammation, Neuroimmunomodulation",
author = "J. Szel{\'e}nyi and E. V{\'i}zi",
year = "2007",
month = "10",
doi = "10.1196/annals.1391.026",
language = "English",
isbn = "157331675X",
volume = "1113",
series = "Annals of the New York Academy of Sciences",
pages = "311--324",
booktitle = "Annals of the New York Academy of Sciences",

}

TY - GEN

T1 - The catecholamine-cytokine balance

T2 - Interaction between the brain and the immune system

AU - Szelényi, J.

AU - Vízi, E.

PY - 2007/10

Y1 - 2007/10

N2 - Cytokines are involved both in various immune reactions and in controlling certain events in the central nervous system (CNS). In our earlier studies, it was shown that monoamine neurotransmitters, released in stress situations, represent a tonic sympathetic control on cytokine production and on the balance of proinflammatory/anti-inflammatory cytokines. Basic and clinical studies have provided evidence that the biophase level of monoamines, determined by the balance of their release and uptake, is involved in the pathophysiology and treatment of depression, while inflammatory mediators might also have a role in its etiology. In this work, we studied the role of changes in norepinephrine (NE) level on the lipopolysaccharide (LPS) evoked tumor necrosis factor (TNF)-α and interleukin (IL)-10 response both in the plasma and in the hippocampus of mice. We demonstrated that the LPS induced TNF-α response is in direct correlation with the biophase level of NE, as it is significantly higher when the release of NE of vesicular origin was completely inhibited in an animal model of depression (reserpine treatment) and it is significantly lower in the case of increasing biophase levels of NE by genetic (NET-KO) or chemical (desipramine) disruption of NE reuptake. IL-10 was changed inversely to TNF-α levels only in the desipramine-treated animals. Our results showed that depression is related both to changes in peripheral and in hippocampal inflammatory cytokine production and to monoamine neurotransmitter levels. Since several anti-inflammatory drugs also have antidepressant effects, we hypothesized that antidepressants are also able to modulate the LPS-induced inflammatory response, which might contribute to their antidepressant effect.

AB - Cytokines are involved both in various immune reactions and in controlling certain events in the central nervous system (CNS). In our earlier studies, it was shown that monoamine neurotransmitters, released in stress situations, represent a tonic sympathetic control on cytokine production and on the balance of proinflammatory/anti-inflammatory cytokines. Basic and clinical studies have provided evidence that the biophase level of monoamines, determined by the balance of their release and uptake, is involved in the pathophysiology and treatment of depression, while inflammatory mediators might also have a role in its etiology. In this work, we studied the role of changes in norepinephrine (NE) level on the lipopolysaccharide (LPS) evoked tumor necrosis factor (TNF)-α and interleukin (IL)-10 response both in the plasma and in the hippocampus of mice. We demonstrated that the LPS induced TNF-α response is in direct correlation with the biophase level of NE, as it is significantly higher when the release of NE of vesicular origin was completely inhibited in an animal model of depression (reserpine treatment) and it is significantly lower in the case of increasing biophase levels of NE by genetic (NET-KO) or chemical (desipramine) disruption of NE reuptake. IL-10 was changed inversely to TNF-α levels only in the desipramine-treated animals. Our results showed that depression is related both to changes in peripheral and in hippocampal inflammatory cytokine production and to monoamine neurotransmitter levels. Since several anti-inflammatory drugs also have antidepressant effects, we hypothesized that antidepressants are also able to modulate the LPS-induced inflammatory response, which might contribute to their antidepressant effect.

KW - Catecholamine

KW - Cytokine

KW - Depression

KW - Inflammation

KW - Neuroimmunomodulation

UR - http://www.scopus.com/inward/record.url?scp=35548958257&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35548958257&partnerID=8YFLogxK

U2 - 10.1196/annals.1391.026

DO - 10.1196/annals.1391.026

M3 - Conference contribution

C2 - 17584982

AN - SCOPUS:35548958257

SN - 157331675X

SN - 9781573316750

VL - 1113

T3 - Annals of the New York Academy of Sciences

SP - 311

EP - 324

BT - Annals of the New York Academy of Sciences

ER -