Peripheral neuroimmune interactions and neuropathic pain

Abstract

Neuropathic pain often results from damage to peripheral nerves, which can mobilize the immune system, as in Guillain-Barré syndrome, postherpetic neuralgia, or trauma. Although most studies focused on detrimental effects of neuroinflammation, recent experimental data provide evidence on analgesic effects of leukocytes. Pain-ameliorating actions involve anti-inflammatory cytokines and immune cell-derived opioid peptides, which activate opioid receptors on peripheral terminals of sensory neurons in injured nerves. In addition, endocannabinoids are present in leukocytes, and mechanisms involved in the resolution of inflammation are mounted, but their significance to neuropathic pain modulation is yet to be examined. Clinical evidence is less compelling, although in some conditions the occurrence of pain seems to be associated with lowered numbers of macrophages or T lymphocytes. This chapter discusses studies addressing both unfavorable and beneficial actions of neuroinflammation in the regulation of painful neuropathies.