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.