Interleukin-1beta: a common thread between inflammation, pain and opioid tolerance

Chronic pain is a major health issue in our society that clearly impacts quality of life. Thirty to forty percent of the population in the United States suffer from chronic pain and its total cost have been estimated at 560-635 billion dollars annually.[1] Even if research progresses to develop novel analgesics, opioids remain the gold standard to treat pain. However, opioid treatment is associated with several adverse side effects including analgesic tolerance and opioid-induced hyperalgesia (OIH). OIH is of major importance and the use of morphine continues to increase. Analgesia tolerance corresponds to a progressive decrease of analgesia produced by a given dose of opioid upon chronic administration, resulting in the need to increase the dosage in order to maintain the initial analgesic effect. OIH usually clinically presents itself as the development of hypersensitivity to painful stimuli. OIH is well established in humans in different types of pain such as post-surgical pain, cancer pain and musculoskeletal pain.[2-4] Hence, clinicians face a dilemma to decided to either treat or not treat chronic pain with opioids which the knowledge of the patient developing pain hypersensitivity that may develop into opioid dependence. OIH is not yet completely understood and different mechanisms have been identified for this adaptive process to occur following opioid administration. These included the sensitization of primary afferent neurons and enhanced release of glutamate, hyperexcitability of second order neurons to excitatory neurotransmitters. However, more recently glial cells have been shown to play an important role in OIH. Receptors expressed in both microglia and Dr. Shekher Mohan is currently an Assistant Professor of Neuropharmacology at Marshall University, School of