Effects of Mood State and Psychosocial Functioning on Plasma Interleukin-6 in Adult Patients before Cardiac Surgery

Ai, Amy L.; Kronfol, Ziad; Seymour, Eric; Bolling, S. F.

doi:10.2190/2elg-rdun-x6tu-fgc8

Cited by 16 publications

(21 citation statements)

References 48 publications

(59 reference statements)

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“…In general, the experience of pain appears to be associated with enhanced release of pro-inflammatory cytokines, which in turn sensitize the nervous system, promoting an amplification of pain transmission(4;5;13;44;84). Indeed, pro-inflammatory cytokines such as interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α) and others show positive associations with pain severity among samples of RA, osteoarthritis, back pain, cardiac, and fibromyalgia patients(2;33;62;68;86;94;95). …”

Section: Introductionmentioning

confidence: 99%

Association of catastrophizing with interleukin-6 responses to acute pain

Edwards

Kronfli

Haythornthwaite

et al. 2008

Pain

181

143

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Catastrophizing exerts its deleterious effects on pain via multiple pathways, and some researchers have reported that high levels of catastrophizing are associated with enhanced physiological reactivity to painful stimulation. In this project, 42 generally healthy adults underwent a series of psychophysical pain testing procedures assessing responses to noxious mechanical, heat, and cold stimuli. Pain-catastrophizing cognitions were assessed prior to and then immediately after the various pain induction procedures. Blood samples were taken at baseline and then at several time points from the end of the procedures to 1 hour post-testing. Samples were assayed for serum levels of cortisol and interleukin-6 (IL-6). Both cortisol and IL-6 increased from baseline during the post-testing period (p's< .05), with cortisol returning to baseline by 1 hour post-testing and IL-6 remaining elevated. Pain catastrophizing, measured immediately after the pain procedures, was unrelated to cortisol reactivity, but was strongly related to IL-6 reactivity (p< .01), with higher levels of catastrophizing predicting greater IL-6 reactivity. In multivariate analyses, the relationship between catastrophizing and IL-6 reactivity was independent of pain ratings. Collectively, these findings suggest that cognitive and emotional responses during the experience of pain can shape pro-inflammatory immune system responses to noxious stimulation. This pathway may represent one important mechanism by which catastrophizing and other psychosocial factors shape the experience of both acute and chronic pain in a variety of settings.

show abstract

Section: Introductionmentioning

confidence: 99%

Association of catastrophizing with interleukin-6 responses to acute pain

Edwards

Kronfli

Haythornthwaite

et al. 2008

Pain

181

143

View full text Add to dashboard Cite

show abstract

“…Patients with autoimmune diseases such as RA, IBD and SLE which are refractory to conventional therapy have been shown to have increased activity and expression of Pgp [22,23]. The prolonged uses of corticosteroids have been associated with an increase in Pgp activity [24], which decreases the response to standard therapies, paradoxically increasing the release of pro-inflammatory cytokines and exacerbating the inflammatory response [22].…”

Section: Mechanisms For Drug Resistancementioning

confidence: 99%

“…The prolonged uses of corticosteroids have been associated with an increase in Pgp activity [24], which decreases the response to standard therapies, paradoxically increasing the release of pro-inflammatory cytokines and exacerbating the inflammatory response [22].…”

Section: Mechanisms For Drug Resistancementioning

confidence: 99%

“…About 90% of circulating glucocorticoids are bound to CBG, preventing its access to the cell. Several studies have shown that during turpentine-inflammation in rats, after endotoxin administration, in the murine model of SLE and in humans with septic shock, CBG levels are decreased [22].…”

Section: P-glycoprotein and Glucocorticoidsmentioning

confidence: 99%

“…cortisol into cortisone) preventing binding to the receptor. Pgp functions as an efflux pump for glucocorticoids [22].…”

Section: P-glycoprotein and Glucocorticoidsmentioning

confidence: 99%

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