Burkholderia cenocepacia infections in CF patients involve heightened 
inflammation, fatal sepsis, and high antibiotic resistance. Proinflammatory 
IL-1β secretion is important in airway inflammation and tissue damage. However, 
little is known about this pathway in macrophages upon B. cenocepacia infection. 
We report here that murine macrophages infected with B. cenocepacia K56-2 
produce proinflammatory cytokine IL-1β in a TLR4 and caspase-1-mediated manner. 
We also determined that the OPS (O antigen) of B. cenocepacia LPS contributes to 
IL-1β production and pyroptotic cell death. Furthermore, we showed that the 
malfunction of the CFTR channel augmented IL-1β production upon B. cenocepacia 
infection of murine macrophages. Taken together, we identified eukaryotic and 
bacterial factors that contribute to inflammation during B. cenocepacia 
infection, which may aid in the design of novel approaches to control pulmonary 
inflammation.