Inflammation and Brain Function - Main Study
Condition: Sickness Behavior
MeSH terms: Inflammation; Illness Behavior
Study type: Interventional

Summary: 
      In this randomized double blind study, 52 healthy participants were injected with either 0.6
      ng/kg body weight or placebo to test if changes in pain sensitivity is associated with change
      in neural activity using BOLD MR scanning.
    

Detailed description: 
      52 healthy participants were included in this randomized double blind study. Participants
      were injected once, and randomized to injection with with the active component or placebo.
      Participants were recruited by advertising and screened through questionnaires and a health
      examination by a physician. They were asked not to engage in strenuous physical activities,
      sleep regular hours and refrain from alcohol the day before the experiment. If the
      participants felt ill, e.g. coming down with a cold, they were instructed to call and were
      rescheduled for a later appointment. C-reactive protein (CRP) was assessed to exclude
      participants having an ongoing infection on the experimental day. Pregnancy was also an
      exclusion criteria and a pregnancy test was administered for all female participants on
      arrival. Pain sensitivity measures were tested at baseline and at peak inflammatory response
      1-2 hours after injection. Both deep and cutaneous pain at threshold and suprathreshold
      noxious levels were tested. Heat- and cold (cutaneous) pain sensitivity was assessed for
      threshold stimuli and intense noxious stimuli, as well as pressure (deep) pain thresholds and
      CPM (descending pain inhibition). These tests were conducted while the participants were in
      the MR-scanner to investigate neural correlates to change in pain sensitivity. Subjects
      filled out questionnaires at baseline, 90 minutes, 3.5 and 5 hours after injection.

      The study and the procedures used in the study are described in detail here:
      https://openarchive.ki.se/xmlui/bitstream/handle/10616/44650/Thesis_Bianka_Karshikoff.pdf?seq
      uence=8&isAllowed=y

      The following papers using data from this study is published:

      Lindstedt F, Karshikoff B, Schalling M, Olgart Hoglund C, Ingvar M, Lekander M & Kosek E.
      Serotonin-1A Receptor Polymorphism (rs6295) Associated with Thermal Pain Perception. PLOS
      ONE. 2012;7(8):e43221. Epub 2012/09/07.

      Karshikoff B, Jensen KB, Kosek E, Kalpouzos G, Soop A, Ingvar M, Olgart Höglund C, Lekander
      M, Axelsson J. Why sickness hurts: A central mechanism for pain induced by peripheral
      inflammation. Brain, Behavior, and Immunity 2016 Oct;57:38-46.

      Lekander M, Karshikoff B, Johansson E, Soop A, Fransson P, Lundström J N, Andreasson A,
      Ingvar M, Petrovic P, Axelsson J/Nilsonne G. Intrinsic functional connectivity of insular
      cortex and symptoms of sickness during acute experimental inflammation. Brain, Behavior, and
      Immunity 2016 Aug;56:34-41.

      Andreasson A, Wicksell RK, Lodin K, Karshikoff B, Axelsson J, Lekander M. A Global Measure of
      Sickness Behavior: Development of the Sickness Questionnaire (SicknessQ). Journal of Health
      Psychology. 2016 Jul 24.

      Karshikoff B, Lekander M, Soop A, Lindstedt F, Ingvar M Kosek E, Olgart Höglund C, & Axelsson
      J. Modality and sex differences in pain sensitivity during human endotoxemia. Brain,
      Behavior, and Immunity. 2015 May;46:35-43
    

Intervention name(s): Endotoxin; Placebo
Intervention type(s): Biological; Biological
Intervention description(s): Endotoxin at 0.6 ng/kg of body weight administered intravenously (Escherichia Coli, Lot nr G3E0609, United States Pharmacopeia Rockville, MD); Saline administered intravenously
Other intervention name(s): LPS; Lipopolysaccharide
Allocation: Randomized
Intervention model: Parallel Assignment
Masking: Triple (Participant, Care Provider, Investigator)
Primary purpose: Basic Science
Keywords: Sickness behavior; Endotoxin; Lipopolysaccharide; Psychoneuroimmunology