Stress of different types increases the proinflammatory load in rheumatoid arthritis
1 Laboratory of Experimental Rheumatology and Neuroendocrino-Immunology, Division of Rheumatology, Department of Internal Medicine I, University Hospital, 93042 Regensburg, Germany
2 Department of Medicine 3, University of Erlangen-Nuremberg, Nikolaus-Fiebiger-Center, 91054 Erlangen, Germany
Arthritis Research & Therapy 2009, 11:114 doi:10.1186/ar2712
See related research article by Edwards et al., http://arthritis-research.com/content/11/3/R61Published: 17 June 2009
Stress in patients with chronic inflammatory diseases such as rheumatoid arthritis (RA) stimulates proinflammatory mechanisms due to the defect of stress response systems (for example, the sympathetic nervous system and the hypothalamic–pituitary–adrenal axis). Among other mechanisms, the loss of sympathetic nerve fibers in inflamed tissue and inadequate cortisol secretion in relation to inflammation lead to an enhanced proinflammatory load in RA. Stress and the subsequent stimulation of inflammation (systemic and local) lead to increased sensitization of pain and further defects of stress response systems (vicious cycle of stress, pain, and inflammation).