Role of interleukin-1 and inflammasomes in oral disease

Inflammation promotes immune cell infiltration into tissues and induces production of pro-inflammatory cytokines that mediate innate immune responses. Acute or temporary inflammation results in the required repair of the inflamed tissues. However, chronic inflammation leads to pathogenesis of inflammatory conditions such as periodontal disease. In periodontal tissues, pro-inflammatory cytokines mediate inflammatory responses and accelerate the bone-resorbing activity of osteoclasts, resulting in destruction of alveolar bone. Levels of interleukin-1 (IL-1), a major pro-inflammatory cytokine that strongly promotes osteoclastic activity, are elevated in oral tissues of patients with periodontitis. Therefore, elucidation of the mechanisms underlying IL-1 production will enhance our understanding of the pathogenesis of periodontal disease.

IL-1 has two isoforms: IL-1α and IL-1β. Both isoforms bind to the same IL-1 receptor and have identical biological activity. Unlike that of IL-1α, the IL-1β precursor is not bioactive. To induce its bioactivity, the IL-1β precursor is cleaved by caspase-1, whose activation is mediated by multiprotein complexes termed inflammasomes. Thus, IL-1β maturation and activity are strictly regulated by inflammasomes. This review highlights the current understanding of the molecular mechanisms underlying IL-1 production and the related inflammasome activity.

Inhibition of IL-1 production or the inflammasomes via their regulatory mechanisms may facilitate prevention or treatment of periodontal disease and other inflammatory diseases.