T E Lacourt1, J H Houtveen2, J J C S Veldhuijzen van Zanten3, J A Bosch4, M T Drayson5, L J P Van Doornen6. 1. Department of Clinical and Health Psychology, Utrecht University, Heidelberglaan 1, 3584 CS Utrecht, The Netherlands; Department of Symptom Research, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 1450, Houston, TX 77030, USA. Electronic address: tlacourt@mdanderson.org. 2. Department of Clinical and Health Psychology, Utrecht University, Heidelberglaan 1, 3584 CS Utrecht, The Netherlands; Department of Psychiatry, University of Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands. 3. School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom. 4. School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom; Department of Clinical Psychology, University of Amsterdam, Weesperplein 4, 1018 XA Amsterdam, The Netherlands; Mannheim Institute of Public Health, Social and Preventive Medicine (MIPH), Mannheim Medical Faculty, University of Heidelberg, Ludolf-Krehl-Strasse 7-11, D-68167 Mannheim, Germany. 5. Division of Immunity and Infection, Medical School, University of Birmingham, Birmingham B15 2TT, United Kingdom. 6. Department of Clinical and Health Psychology, Utrecht University, Heidelberglaan 1, 3584 CS Utrecht, The Netherlands.
Abstract
INTRODUCTION: Experimental animal studies provided evidence for a synergistic effect of immunological and psychological stressors on subsequent sickness behaviours. Up to now, little corroborating evidence for such synergy exists for humans, in whom it may provide a mechanism leading to the expression of functional somatic symptoms. The aim of the present study was to determine an interaction between stress(-vulnerability) and an immunological activation on experimental pain sensitivity, i.e., pressure pain threshold and tolerance in healthy humans. METHODS: In healthy female participants (n=25, mean age 22.3 years), negative affectivity (NA) and experienced stress were assessed by questionnaire before receiving aSalmonella typhi vaccine or saline control in a randomized blinded cross-over design. Pressure pain threshold was assessed at the lower back and calves and pain tolerance was assessed at the thumbnail, before and six hours after each injection. RESULTS: Vaccination induced leukocytosis (+100%) and increased serum IL-6 (+670%). NA predicted decreased pain tolerance after vaccination (β=-.57, p=.007), but not after placebo (β=.25, p=.26). Post-hoc analyses also demonstrated an association with administration order. DISCUSSION: NA moderated the effects of inflammation on pain tolerance. This finding is consistent with a synergistic model whereby inflammation may lower the threshold for pain reporting in individuals with increased vulnerability for somatic symptom reporting.
RCT Entities:
INTRODUCTION: Experimental animal studies provided evidence for a synergistic effect of immunological and psychological stressors on subsequent sickness behaviours. Up to now, little corroborating evidence for such synergy exists for humans, in whom it may provide a mechanism leading to the expression of functional somatic symptoms. The aim of the present study was to determine an interaction between stress(-vulnerability) and an immunological activation on experimental pain sensitivity, i.e., pressure pain threshold and tolerance in healthy humans. METHODS: In healthy female participants (n=25, mean age 22.3 years), negative affectivity (NA) and experienced stress were assessed by questionnaire before receiving a Salmonella typhi vaccine or saline control in a randomized blinded cross-over design. Pressure pain threshold was assessed at the lower back and calves and pain tolerance was assessed at the thumbnail, before and six hours after each injection. RESULTS: Vaccination induced leukocytosis (+100%) and increased serum IL-6 (+670%). NA predicted decreased pain tolerance after vaccination (β=-.57, p=.007), but not after placebo (β=.25, p=.26). Post-hoc analyses also demonstrated an association with administration order. DISCUSSION: NA moderated the effects of inflammation on pain tolerance. This finding is consistent with a synergistic model whereby inflammation may lower the threshold for pain reporting in individuals with increased vulnerability for somatic symptom reporting.
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