NLRP3 inflammasome plays a redundant role with caspase 8 to promote IL-1β–mediated osteomyelitis

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Abstract
Significance: IL-1 is a pleiotropic cytokine involved in a myriad of autoinflammatory disorders. In proline-serine-threonine phosphatase-interacting protein 2 (Pstpip2cmo) mice, IL-1β provokes autoinflammatory osteomyelitis. Here, we demonstrated the redundant roles of Nod like receptor family, pyrin domain containing 3 (NLRP3) inflammasome with caspase 8 in the processing of IL-1β inPstpip2cmomice. Identification of redundancy between NLRP3 inflammasome and caspase 8 is fundamental in our understanding of the inflammasomes and alternative modes of IL-1β regulation in osteomyelitic disease. Moreover, IL-1β signaling connects distinct compartments in promoting the disease, identifying previously unidentified checkpoints that could be targeted for therapeutic purposes in similar disease settings. Thus, our studies have unraveled the complex IL-1β regulatory network in vivo in a mouse model of osteomyelitis that will be useful for autoinflammatory diseases in general.

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