NOCICEPTION AND ROLE OF IMMUNE SYSTEM

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Analgesic Effects of Immune system
On a contrary to the villainous projection of immune system; evidences also support the analgesic effects of immune cells and mediators in painful conditions. In inflammation, leucocytes containing opioid peptides migrate into the tissue. This migration is controlled by chemokines and adhesion molecules. Neurokinins, such as, substance P also contribute to the recruitment of these “analgesic” cells. Opioid peptides release from granulocytes is stimulated by chemokines, such as; CXCL1 and CXCL2.8 Recent research has also confirmed expression of endorphins in T-cells, macrophages and fibroblast. Additionally, Endothelin-B receptor activation during inflammation leads to release of β-endorphin from keratinocytes. Released opioids bind to opioid receptors on peripheral nerve terminals, which counteract inflammatory pain. Additionally, expression of opioid receptors on peripheral nerves increase in response to inflammation and this further exaggerates analgesic effect of endogenous immune derived opioid peptides.
Certain specialized mediators of inflammation (lipoxins, resolvins and neuroprotectins) aid in resolution of acute inflammatory state (fig.7). It is now clear that “anti-inflammatory” and “pro-resolution” effects of these molecules are independent and well pronounced phenomena. Moreover, leukocytes interact with other cells like platelets, endothelium, epithelial cells and fibroblast to switch their phenotype from pro-inflammatory to anti-inflammatory, thus restoring homoeostasis. Lipoxins (LXA4 and LXB4) are generated from arachidonic acid via the phospholipase A2–lipoxygenase pathway during cell–cell interactions. It facilitates resolution of inflammation by stopping recruitment of neut...

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...t explanations for chronic and neuropathic conditions; thus suggesting future work towards exploring this scope.
Knocking out various immune responses (and mediators) provides an inconclusive but effective method to manage pain. Additionally, glial modulators and their efficacy confirm glia mediated immune system involvement in nociception. On the other hand, further understanding of involvement of immune system reveals independent anti-inflammatory and pro-resolution roles of immune mediators. These approaches altogether exposes a new domain for pharmacological exploration in development of safer and effective analgesics. To summarize, our understanding of pain and role of neuro-immune interface is still juvenile. Future work in understanding the intricacies of nervous system and immune system promises a premise for long waited effective pain management strategies.

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