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

Samuel B Chivers1, Mary Ann Andrade2, Robert J Hammack2

  • 1Department of Oral and Maxillofacial Surgery, University of Texas Health San Antonio, San Antonio, TX, USA.

Science Signaling
|July 30, 2024
PubMed

Insights

Obstructive sleep apnea (OSA) causes chronic pain by triggering inflammation and nerve sensitization through intermittent hypoxia. Targeting hypoxia or macrophages may alleviate pain in OSA patients.

Area of Science:

  • Neuroscience
  • Immunology
  • Sleep Medicine

Background:

  • Obstructive sleep apnea (OSA) is linked to chronic musculoskeletal pain.
  • The underlying mechanisms connecting OSA and pain are not fully understood.

Purpose of the Study:

  • To investigate the mechanism linking chronic intermittent hypoxia (CIH), mimicking OSA, to persistent pain.
  • To explore the role of inflammation and immune cells in CIH-induced pain.

Main Methods:

  • Mice were exposed to CIH for 14 days.
  • Pain behaviors, biochemical markers, macrophage recruitment, cytokine levels, and nociceptor sensitization were assessed.
  • Peripheral macrophages were ablated to test their role.

Main Results:

  • CIH induced pain behaviors and hyperalgesic priming in mice.
  • CIH increased macrophage recruitment to sensory tissues and circulating inflammatory cytokines.
  • Nociceptor sensitization was observed, and macrophage ablation blocked CIH-induced pain priming.

Conclusions:

  • CIH, not just sleep fragmentation, drives pain in a mouse model of OSA.
  • Macrophage signaling plays a critical role in mediating CIH-induced pain.
  • Therapeutic strategies targeting hypoxia or macrophage pathways may treat OSA-associated pain.

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