Stress activation of cellular markers of inflammation in rheumatoid arthritis: Protective effects of tumor necrosis factor α antagonists
Article first published online: 31 JAN 2008
Copyright © 2008 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 58, Issue 2, pages 376–383, February 2008
How to Cite
Motivala, S. J., Khanna, D., FitzGerald, J. and Irwin, M. R. (2008), Stress activation of cellular markers of inflammation in rheumatoid arthritis: Protective effects of tumor necrosis factor α antagonists. Arthritis & Rheumatism, 58: 376–383. doi: 10.1002/art.23165
- Issue published online: 31 JAN 2008
- Article first published online: 31 JAN 2008
- Manuscript Accepted: 26 OCT 2007
- Manuscript Received: 13 JUN 2007
- NIH. Grant Numbers: T32-MH-18399, HL-079955, AG-026364, CA-10014152, RR-00827
- General Clinical Research Centers Program
- University of California, Los Angeles
- Cousins Center for Psychoneuroimmunology
- Arthritis Foundation
- Scleroderma Foundation
Psychological stress is thought to aggravate disease activity in rheumatoid arthritis (RA), although the physiologic mechanisms are unclear. Tumor necrosis factor α (TNFα) is an inflammatory cytokine involved in the exacerbation of RA, and TNFα antagonists have emerged as efficacious treatments. The purpose of this study was to determine whether RA patients show increased monocyte production of TNFα following acute psychological stress and whether such responses are abrogated in RA patients taking TNFα antagonists.
A standardized stress task was administered to 3 groups of subjects: RA patients taking TNFα antagonists, RA patients not taking such medications, and healthy controls. Lipopolysaccharide-stimulated monocyte production of inflammatory cytokines was repeatedly measured using intracellular staining and flow cytometry. Subjective stress, cardiovascular responses, adrenocorticotropic hormone (ACTH) levels, and cortisol levels were also measured.
The stress task induced increases in subjective stress, cardiovascular activity, and levels of ACTH and cortisol, with similar responses in the 3 groups. In addition, the stress task induced a significant increase (P < 0.001) in monocyte production of TNFα among RA patients who were not taking TNFα antagonists. However, monocyte production of TNFα did not change following psychological stress in RA patients taking TNFα antagonists or in healthy controls.
Brief psychological stress can trigger increased stimulated monocyte production of TNFα in RA patients. The use of TNFα antagonists protects against stress activation of cellular markers of inflammation in RA patients.