Provoked cytokine response is not associated with distress or induced secondary hyperalgesia in people with suppressed HIV.

ABSTRACT: Psychological distress predicts the onset and worsening of persistent pain, but the mechanisms that underpin this influence are poorly understood. Pro-inflammatory signalling is a plausible mechanistic link, given its known connections to distress, pain, and neural upregulation. Sustained distress may prime the inflammatory system to respond more strongly to a phasic noxious challenge, supporting neuroimmune upregulation of central nociceptive signalling and persistent pain. This cross-sectional study tested the hypotheses that in vitro endotoxin-provoked expression of typically pro-inflammatory cytokines (IL1β, IL6) is a partial mediator between distress and persistent pain, and that it is associated with the secondary hyperalgesia response to an experimental noxious challenge, in

SUBMITTER: Madden VJ 

PROVIDER: S-EPMC11838944 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature