My research falls within the broad field of Psychoneuroimmunology (PNI), which looks at interactions among behavior, nervous, endocrine, and immune systems. My research focuses on the interactions among opiates, pain, and the immune system, and involves several lines of research:
In recent years we have examined the hypothesis that proinflammatory cytokines (particularly interleukin-1; IL-1) are involved in pain sensitivity. We have shown that IL-1 plays a pain-enhancing (hyperalgesic) role in a normal, non-inflamed state, as well as in several animal pain models, including neuropathic pain, and postoperative pain. Furthermore, we have described interesting interactions between the analgesic effects of morphine and the anti-analgesic effects of IL-1, showing that elevated levels of IL-1 counter-regulate morphine analgesia and thus may be involved in the development of opiate tolerance. Indeed, recent findings indicate that morphine produced elevation of IL-1 levels, which serves to limit the duration and extent of morphine analgesia and which underlies the development of tolerance.
Inflammatory condition modulates pain sensitivity via peripheral and central mechanisms, most of which are associated with hyperalgesia and fall under the term "peripheral and central sensitization". Accumulating evidence, however, suggests that inflammation, especially peripheral inflammation, can also induce hypo-algesia, via changes to peripheral opioids mechanisms. Using a mouse model of peripheral inflammation-induced chronic pain, we have shown that morphine plays an anti-inflammatory role in a state of chronic peripheral inflammation. Furthermore, the inflammatory state is associated with potentiated morphine analgesia.