NF-kB activation is responsible for causing the inflammation that results in neuropathic pain
Neuropathic pain has sometimes been referred to as non-inflammatory pain. But there is now overwhelming evidence that inflammation is a crucial, probably essential, contributor to neuropathic pain – and NF-kB is the Master Switch controlling that inflammation.
Tumor necrosis factor receptor 1 induces interleukin-6 upregulation through NF-kappaB in a rat neuropathic pain model
Summary of the abstract
Peripheral nerve injury resulting in neuropathic pain induces the upregulation of interleukin (IL)-6 and tumor necrosis factor-alpha, which binds to tumor necrosis factor receptor 1 (TNFR1) and induces NF-kappaB and p38 MAPK activation in the spinal cord and dorsal root ganglia (DRG).
We here investigated whether TNFR1 regulates IL-6 expression through NF-kappaB or p38 MAPK.
NF-kappaB decoy, but not p38 MAPK inhibitor, reduced elevated IL-6 expression in the spinal cord and DRG. Therefore, these data suggest that TNFR1 induces IL-6 upregulation and neuropathic pain through NF-kappaB, but not p38 MAPK activation in the spinal cord and DRG.
In neuropathic pain, NF-kB is the critical pathway, not MAPK
IL-6 is here presumably acting as a pro-inflammatory mediator that is responsible, at least in part, for promoting the continuation of pain signals in neuropathic pain.
It was found to be regulated by NF-kB.