Science Transl. Med. https://doi.org/10.1126/scitranslmed.abj9954 (2022)
Lower back pain often develops into a chronic condition. The mechanism that underlies this transition is incompletely understood, but it is thought to involve activation of immune cells. To investigate this mechanism, the authors of a study published in Science Translational Medicine examined peripheral blood immune cells from 98 patients with lower back pain in the acute stage and again three months later, by which time the pain had resolved in 49 patients and had become persistent in the other 49 patients. Transcriptomics data indicated that in the acute stage, expression of biological pathways related to inflammatory responses was higher in patients whose pain later resolved than in those in whom it did not. Three months later, the ‘resolved’ group had 1,700 differentially expressed genes, a decrease in the proportion of neutrophils, and downregulation of inflammatory response pathways compared with the acute stage, whereas the ‘persistent’ group showed no significant changes over time. The authors replicated these findings in patients with a different musculoskeletal pain condition. In mouse models of inflammatory pain, dexamethasone or a nonsteroidal anti-inflammatory drug (NSAID) reduced allodynia acutely but prolonged the duration of the pain episode. Depletion of neutrophils had the same effect, whereas an increase in neutrophils or the neutrophil-released proteins S1000A8 or S1000A9 prevented the dexamethasone-induced prolongation of allodynia. In addition, data from the UK Biobank indicated that in people with acute back pain, self-reported use of NSAIDs — but not any other analgesic medication — increased the risk of developing chronic pain. Together, these findings suggest that enhanced inflammatory responses in the acute pain stage may protect against pain becoming chronic and raise the intriguing possibility that use of anti-inflammatory drugs for acute lower back pain may be counterproductive.
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