NFKB1 and infection: Further, another study using Bpm-infected primary human macrophages implicated the T3SS-3 dependent inflammasome activation and IFN-γ induced immune mechanisms as a defense mechanism against the pathogen, although reduced intracellular Bpm loads were observed, the inflammatory response was not completely abolished.44 Now, we present evidence that a functional T6SS is required to block NF-κB activation during Bpm infection of IECs and this system seems to work in conjunction with the T3SS to modulate the inflammatory response observed during infection of host cells.