Proinflammatory cytokines and sickness behavior in rheumatic diseases

Dianne Lorton, C. L. Lubahn, A. J. Zautra, D. L. Bellinger

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

This review describes mechanisms of immune-to-brain signaling that may contribute to disease-related changes in mood, affect and behavior in chronic inflammatory rheumatic diseases. The central nervous system (CNS) modulates immune function by signaling target cells of the immune system through autonomic and neuroendocrine pathways. These immune cells relay information back to autonomic, limbic and cortical areas of the CNS to affect neural activity and consequently modify behavior, hormone release and autonomic function [1,2]. In this manner, immune cells function as a sense organ, informing the CNS of peripheral events relating to infection and irjury [3]. Equally important, homeostatic mechanism are needed at all levels to turn off the immune response when the pathogen and injurious condition are eliminated and the repair process is completed. In individuals with chronic inflammatory diseases, such as rheumatoid arthritis (RA), there is a failure of the homeostatic regulation leading to long-term immune activation that has serious health consequences. Rheumatic disorders constitute a challenge to major psychological adaptation resources leading to higher rates of psychological disorders compared with the general population. Thus the relationship between disease pathology and psychological well being is complex.

Original languageEnglish (US)
Pages (from-to)1242-1260
Number of pages19
JournalCurrent Pharmaceutical Design
Volume14
Issue number13
StatePublished - May 2008

Fingerprint

Illness Behavior
Rheumatic Diseases
Central Nervous System
Cytokines
Sense Organs
Psychology
Autonomic Pathways
Psychological Adaptation
Immune System
Rheumatoid Arthritis
Chronic Disease
Hormones
Pathology
Health
Brain
Infection
Population

Keywords

  • Cytokines
  • Immune system
  • Nervous system
  • Rheumatoid arthritis
  • Sickness behavior
  • Signaling

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Lorton, D., Lubahn, C. L., Zautra, A. J., & Bellinger, D. L. (2008). Proinflammatory cytokines and sickness behavior in rheumatic diseases. Current Pharmaceutical Design, 14(13), 1242-1260.

Proinflammatory cytokines and sickness behavior in rheumatic diseases. / Lorton, Dianne; Lubahn, C. L.; Zautra, A. J.; Bellinger, D. L.

In: Current Pharmaceutical Design, Vol. 14, No. 13, 05.2008, p. 1242-1260.

Research output: Contribution to journalArticle

Lorton, D, Lubahn, CL, Zautra, AJ & Bellinger, DL 2008, 'Proinflammatory cytokines and sickness behavior in rheumatic diseases', Current Pharmaceutical Design, vol. 14, no. 13, pp. 1242-1260.
Lorton D, Lubahn CL, Zautra AJ, Bellinger DL. Proinflammatory cytokines and sickness behavior in rheumatic diseases. Current Pharmaceutical Design. 2008 May;14(13):1242-1260.
Lorton, Dianne ; Lubahn, C. L. ; Zautra, A. J. ; Bellinger, D. L. / Proinflammatory cytokines and sickness behavior in rheumatic diseases. In: Current Pharmaceutical Design. 2008 ; Vol. 14, No. 13. pp. 1242-1260.
@article{4914a7c5320b47a18cbac1004d2a761d,
title = "Proinflammatory cytokines and sickness behavior in rheumatic diseases",
abstract = "This review describes mechanisms of immune-to-brain signaling that may contribute to disease-related changes in mood, affect and behavior in chronic inflammatory rheumatic diseases. The central nervous system (CNS) modulates immune function by signaling target cells of the immune system through autonomic and neuroendocrine pathways. These immune cells relay information back to autonomic, limbic and cortical areas of the CNS to affect neural activity and consequently modify behavior, hormone release and autonomic function [1,2]. In this manner, immune cells function as a sense organ, informing the CNS of peripheral events relating to infection and irjury [3]. Equally important, homeostatic mechanism are needed at all levels to turn off the immune response when the pathogen and injurious condition are eliminated and the repair process is completed. In individuals with chronic inflammatory diseases, such as rheumatoid arthritis (RA), there is a failure of the homeostatic regulation leading to long-term immune activation that has serious health consequences. Rheumatic disorders constitute a challenge to major psychological adaptation resources leading to higher rates of psychological disorders compared with the general population. Thus the relationship between disease pathology and psychological well being is complex.",
keywords = "Cytokines, Immune system, Nervous system, Rheumatoid arthritis, Sickness behavior, Signaling",
author = "Dianne Lorton and Lubahn, {C. L.} and Zautra, {A. J.} and Bellinger, {D. L.}",
year = "2008",
month = "5",
language = "English (US)",
volume = "14",
pages = "1242--1260",
journal = "Current Pharmaceutical Design",
issn = "1381-6128",
publisher = "Bentham Science Publishers B.V.",
number = "13",

}

TY - JOUR

T1 - Proinflammatory cytokines and sickness behavior in rheumatic diseases

AU - Lorton, Dianne

AU - Lubahn, C. L.

AU - Zautra, A. J.

AU - Bellinger, D. L.

PY - 2008/5

Y1 - 2008/5

N2 - This review describes mechanisms of immune-to-brain signaling that may contribute to disease-related changes in mood, affect and behavior in chronic inflammatory rheumatic diseases. The central nervous system (CNS) modulates immune function by signaling target cells of the immune system through autonomic and neuroendocrine pathways. These immune cells relay information back to autonomic, limbic and cortical areas of the CNS to affect neural activity and consequently modify behavior, hormone release and autonomic function [1,2]. In this manner, immune cells function as a sense organ, informing the CNS of peripheral events relating to infection and irjury [3]. Equally important, homeostatic mechanism are needed at all levels to turn off the immune response when the pathogen and injurious condition are eliminated and the repair process is completed. In individuals with chronic inflammatory diseases, such as rheumatoid arthritis (RA), there is a failure of the homeostatic regulation leading to long-term immune activation that has serious health consequences. Rheumatic disorders constitute a challenge to major psychological adaptation resources leading to higher rates of psychological disorders compared with the general population. Thus the relationship between disease pathology and psychological well being is complex.

AB - This review describes mechanisms of immune-to-brain signaling that may contribute to disease-related changes in mood, affect and behavior in chronic inflammatory rheumatic diseases. The central nervous system (CNS) modulates immune function by signaling target cells of the immune system through autonomic and neuroendocrine pathways. These immune cells relay information back to autonomic, limbic and cortical areas of the CNS to affect neural activity and consequently modify behavior, hormone release and autonomic function [1,2]. In this manner, immune cells function as a sense organ, informing the CNS of peripheral events relating to infection and irjury [3]. Equally important, homeostatic mechanism are needed at all levels to turn off the immune response when the pathogen and injurious condition are eliminated and the repair process is completed. In individuals with chronic inflammatory diseases, such as rheumatoid arthritis (RA), there is a failure of the homeostatic regulation leading to long-term immune activation that has serious health consequences. Rheumatic disorders constitute a challenge to major psychological adaptation resources leading to higher rates of psychological disorders compared with the general population. Thus the relationship between disease pathology and psychological well being is complex.

KW - Cytokines

KW - Immune system

KW - Nervous system

KW - Rheumatoid arthritis

KW - Sickness behavior

KW - Signaling

UR - http://www.scopus.com/inward/record.url?scp=47349115734&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=47349115734&partnerID=8YFLogxK

M3 - Article

VL - 14

SP - 1242

EP - 1260

JO - Current Pharmaceutical Design

JF - Current Pharmaceutical Design

SN - 1381-6128

IS - 13

ER -