A adenosine receptor (AAR) agonists have emerged as potent relievers of neuropathic pain by a T cell-mediated production of IL-10. The H histamine receptor (HR), also implicated in pain modulation, is expressed on T cells playing a preeminent role in its activation and release of IL-10. To improve the therapeutic opportunities, this study aimed to verify the hypothesis of a possible cross-talk between AAR and HR in the resolution of neuropathic pain. In the mouse model of Chronic Constriction Injury (CCI), the acute intraperitoneal co-administration of the AAR agonist IB-MECA (0.5 mg/kg) and the HR agonist VUF 8430 (10 mg/kg), were additive in counteracting mechano-allodynia increasing IL-10 plasma levels. In HR mice, IB-MECA activity was reduced, lower pain relief and lower modulation of plasma IL-1β, TNF-α, IL-6 and IL-10 were shown. The complete anti-allodynia effect of IB-MECA in HR mice was restored after intravenous administration of CD4 T cells obtained from naïve wild type mice. In conclusion, a role of the histaminergic system in the mechanism of AAR-mediated neuropathic pain relief was suggested highlighting the driving force evoked by CD4 T cells throughout IL-10 up-regulation.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8533073 | PMC |
http://dx.doi.org/10.3390/biom11101447 | DOI Listing |
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