The cytokine cascade in pain and inflammatory processes is a tremendously complex system, involving glial, immune, and neuronal cell interactions. IL-1beta is a pro-inflammatory cytokine that has been implicated in pain, inflammation and autoimmune conditions. This review will focus on studies that shed light on the critical role of IL-1beta in various pain states, including the role of the intracellular complex, the inflammasome, which regulates IL-1beta production. Evidence will be presented demonstrating the importance of IL-1beta in both the induction of pain and in the maintenance of pain in chronic states, such as after nerve injury. Additionally, the involvement of IL-1beta as a key mediator in the interaction between glia and neurons in pain states will be discussed. Taken together, the evidence presented in the current review showing the importance of IL-1beta in animal and human pain states, suggests that blockade of IL-1beta be considered as a therapeutic opportunity.
