Peripheral macrophages contribute to nociceptor priming in mice with chronic intermittent hypoxia

Samuel B. Chivers, Mary Ann Andrade, Robert J. Hammack, John Shannonhouse, Ruben Gomez, Yan Zhang, Brian Nguyen, Pankil Shah, Yu Shin Kim, Glenn M. Toney, Nathaniel A. Jeske

Research output: Contribution to journalArticlepeer-review

Abstract

Obstructive sleep apnea (OSA) is a prevalent sleep disorder that is associated with increased incidence of chronic musculoskeletal pain. We investigated the mechanism of this association in a mouse model of chronic intermittent hypoxia (CIH) that mimics the repetitive hypoxemias of OSA. After 14 days of CIH, both male and female mice exhibited behaviors indicative of persistent pain, with biochemical markers in the spinal cord dorsal horn and sensory neurons of the dorsal root ganglia consistent with hyperalgesic priming. CIH, but not sleep fragmentation alone, induced an increase in macrophage recruitment to peripheral sensory tissues (sciatic nerve and dorsal root ganglia), an increase in inflammatory cytokines in the circulation, and nociceptor sensitization. Peripheral macrophage ablation blocked CIH-induced hyperalgesic priming. The findings suggest that correcting the hypoxia or targeting macrophage signaling might suppress persistent pain in patients with OSA.

Original languageEnglish (US)
Article numbereadn8936
JournalScience signaling
Volume17
Issue number847
DOIs
StatePublished - Jul 30 2024

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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