Opioids affect inflammation and the immune system

Neurogenic inflammation, with its associated hyperalgesia, is linked to release of neuropeptide mediators including substance P, calcitonin gene-related peptide and corticotrophin-releasing factor. The release of substance P may be modified by opioid receptors on afferent nerve terminals. It is known to be a major mediator of neurogenic inflammation in synovia and is implicated in lymphocyte proliferation and arthritic bone changes. However, opioids may inhibit plasma extravasation and appear to decrease substance P r e l e a s e . Opioid peptides are found in inflamed tissues, released early by interleukin-1 and later by a corticotrophin-releasing factor effect. Opioids appear to interact with interleukins and may act as signalling molecules between immunologically active cells. Endogenous opioids tend to stimulate and exogenous opioids tend to suppress the immune system; information from infections in opioid addicts suggests that this has clinical signific a n c e . Thus, the effect of opioids in modifying the peripheral inflammatory response indicates an analgesic potential at peripheral afferent receptors.