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. Here, IFNG is linked to infection.