CXCL16 mediates nociception and inflammation in murine post-traumatic osteoarthritis DOI
Lindsey Lammlin, S Redding, Alexander J. Knights

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown

Опубликована: Апрель 16, 2025

Abstract This study investigates the role of chemokine CXCL16 and its receptor, CXCR6, in post-traumatic osteoarthritis (PTOA) joint nociception, highlighting potential targeting CXCL16-CXCR6 axis for therapeutically managing inflammation pain. Following injury mice, signaling is activated synovium, driven by synovial fibroblasts macrophages. Human OA synovium also exhibited increased CXCR6 gene expression. stimulated a pro-inflammatory response macrophages, contrasting with an anti-inflammatory observed mesenchymal progenitor cells. In repeated intra-articular injections induced histological synovitis sex-dependent activation inflammatory fibrotic transcriptional programs synovium. Repeated knee hyperalgesia, which was mitigated co-administration antagonist, ML339. A single injection acute hyperalgesia as early 30 minutes post-injection, completely abrogated ML339 co-treatment, suggesting direct binding to nociceptor-expressed CXCR6. murine PTOA model, systemic antagonism alleviated altered circulating immune cell profiles. Direct stimulation mouse dorsal root ganglion-derived nociceptive neurons rapid calcium signaling, abolished co-treatment These findings establish regulator identifies mechanism key mediating pain-related behaviors nociceptor activation, offering therapeutic target PTOA-related pain management. One Sentence Summary regulates mediates nociception via osteoarthritis.

Язык: Английский

CXCL16 mediates nociception and inflammation in murine post-traumatic osteoarthritis DOI
Lindsey Lammlin, S Redding, Alexander J. Knights

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown

Опубликована: Апрель 16, 2025

Abstract This study investigates the role of chemokine CXCL16 and its receptor, CXCR6, in post-traumatic osteoarthritis (PTOA) joint nociception, highlighting potential targeting CXCL16-CXCR6 axis for therapeutically managing inflammation pain. Following injury mice, signaling is activated synovium, driven by synovial fibroblasts macrophages. Human OA synovium also exhibited increased CXCR6 gene expression. stimulated a pro-inflammatory response macrophages, contrasting with an anti-inflammatory observed mesenchymal progenitor cells. In repeated intra-articular injections induced histological synovitis sex-dependent activation inflammatory fibrotic transcriptional programs synovium. Repeated knee hyperalgesia, which was mitigated co-administration antagonist, ML339. A single injection acute hyperalgesia as early 30 minutes post-injection, completely abrogated ML339 co-treatment, suggesting direct binding to nociceptor-expressed CXCR6. murine PTOA model, systemic antagonism alleviated altered circulating immune cell profiles. Direct stimulation mouse dorsal root ganglion-derived nociceptive neurons rapid calcium signaling, abolished co-treatment These findings establish regulator identifies mechanism key mediating pain-related behaviors nociceptor activation, offering therapeutic target PTOA-related pain management. One Sentence Summary regulates mediates nociception via osteoarthritis.

Язык: Английский

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