Studies have suggested that silver nanoparticles can augment the cellular immune responses of cells and thus may contribute to immunopathology, especially as an autoinflammatory disorder. This study examines the interaction of silver nanoparticles with a co-culture of alveolar macrophages and lung epithelial cells to determine if the nanoparticles are capable of activating the inflammasome for sustained production of the pro-inflammatory cytokine interleukin-1beta. It is demonstrated here that interleukin-1beta is upregulated, both the transcript and the mature protein, following 24 hour exposure to 10 nm silver, but that caspase-1 function is downregulated, which prevents confirmation of the inflammasome activity. However, significant upregulation of interleukin-1beta is the contributing factor to many autoinflammatory disorders, indicating that prolonged exposure to silver nanoparticles, even at sub-lethal doses, could potentially cause pathological damage to the host through inflammation.