Chemokine (c-c motif) receptor 2 mediates mechanical and cold hypersensitivity in sickle cell disease mice.
作者： Katelyn E. Sadler , Katherine J. Zappia , Crystal L. OʼHara , Sarah N. Langer , Andy D. Weyer
DOI: 10.1097/J.PAIN.0000000000001253
关键词: Chemokine receptor 、 CCL2 、 Chemokine 、 Immunology 、 CCR2 、 TRPV1 、 Chronic pain 、 CCR4 、 Medicine 、 Proinflammatory cytokine
摘要: Approximately one-third of individuals with sickle cell disease (SCD) develop chronic pain. This debilitating pain is inadequately treated because the underlying mechanisms driving are poorly understood. In addition to persistent pain, patients SCD also in a tonically proinflammatory state. Previous studies have revealed that there elevated plasma levels many inflammatory mediators including chemokine (c-c motif) ligand 2 (CCL2) SCD. Using transgenic mouse model SCD, we investigated contributions CCL2 signaling SCD-related Inhibition receptor (CCR2), but not CCR4, alleviated behavioral mechanical and cold hypersensitivity Furthermore, acute CCR2 blockade reversed both vitro responsiveness sensory neurons an agonist TRPV1, neuronal ion channel previously implicated These results provide insight into immune-mediated regulation could inform future development analgesics or therapeutic measures prevent
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