| Autor: |
Chivers, Samuel B., Andrade, Mary Ann, Hammack, Robert J., Shannonhouse, John, Gomez, Ruben, Zhang, Yan, Nguyen, Brian, Shah, Pankil, Kim, Yu Shin, Toney, Glenn M., Jeske, Nathaniel A. |
| Předmět: |
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| Zdroj: |
Science Signaling; 7/30/2024, Vol. 17 Issue 847, p1-13, 13p |
| Abstrakt: |
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. Editor's summary: Chronic pain is associated with both obstructive sleep apnea and sleep deprivation, which is a consequence of sleep apnea. Chivers et al. found that mice exposed during sleep to chronic episodes of hypoxia—but not those merely roused from sleep as often—were more sensitive to heat and touch. Hypoxia activated peripheral macrophages in the circulation and promoted their recruitment into sensory nerve tissues, whose sensitivity was increased by macrophage-released cytokines. The findings identify a target to potentially reduce chronic pain in patients with sleep apnea. —Leslie K. Ferrarelli [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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