Pain-like behavior in the collagen antibody-induced arthritis model is regulated by lysophosphatidic acid and activation of satellite glia cells.

التفاصيل البيبلوغرافية
العنوان: Pain-like behavior in the collagen antibody-induced arthritis model is regulated by lysophosphatidic acid and activation of satellite glia cells.
المؤلفون: Su, Jie, Krock, Emerson, Barde, Swapnali, Delaney, Ada, Ribeiro, Johnny, Kato, Jungo, Agalave, Nilesh, Wigerblad, Gustaf, Matteo, Rosalia, Sabbadini, Roger, Josephson, Anna, Chun, Jerold, Kultima, Kim, Peyruchaud, Olivier, Hökfelt, Tomas, Svensson, Camilla I
المصدر: Brain, behavior, and immunity. 101:214-230
مصطلحات موضوعية: Dorsal root ganglia, Inflammation, Neuropathic pain, Rheumatoid arthritis, autoantibodies, lipid signaling
الوصف: Inflammatory and neuropathic-like components underlie rheumatoid arthritis (RA)-associated pain and lysophosphatidic acid (LPA) is linked to both joint inflammation in RA patients and to neuropathic pain. Thus, we investigated a role for LPA signalling using the collagen antibody-induced arthritis (CAIA) model. Pain-like behavior during the inflammatory phase and the late, neuropathic-like phase of CAIA was reversed by a neutralizing antibody generated against LPA and by an LPA1/3 receptor inhibitor, but joint inflammation was not affected. Autotaxin, an LPA synthesizing enzyme was upregulated in dorsal root ganglia (DRG) neurons during both CAIA phases, but not in joints or spinal cord. Late-phase pronociceptive neurochemical changes in the DRG were blocked in Lpar1 receptor deficient mice and reversed by LPA neutralization. In vitro and in vivo studies indicated that LPA regulates pain-like behavior via the LPA1 receptor on satellite glia cells (SGCs), which is expressed by both human and mouse SGCs in the DRG. Furthermore, CAIA-induced SGC activity is reversed by phospholipid neutralization and blocked in Lpar1 deficient mice. Our findings suggest that the regulation of CAIA-induced pain-like behavior by LPA signalling is a peripheral event, associated with the DRGs and involving increased pronociceptive activity of SGCs, which in turn act on sensory neurons.
وصف الملف: electronic
URL الوصول: https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-465021
https://doi.org/10.1016/j.bbi.2022.01.003
https://uu.diva-portal.org/smash/get/diva2:1628877/FULLTEXT01.pdf
قاعدة البيانات: SwePub
الوصف
تدمد:08891591
10902139
DOI:10.1016/j.bbi.2022.01.003