Clinical isolates of antimicrobial resistant Enterobacter species can persist in human macrophages without replication and overt cellular cytotoxicity.

Background: Enterobacter species are opportunistic, multidrug resistant Gram-negative bacteria associated with morbidity and mortality worldwide. Since very little is known about the infection biology of Enterobacter spp., we investigated the intracellular trafficking of a subset of Enterobacter clinical isolates, including colistin-resistant strains, within human macrophages, and determined the macrophage response to the intracellular infection.

The Achromobacter type 3 secretion system drives pyroptosis and immunopathology via independent activation of NLRC4 and NLRP3 inflammasomes.

How the opportunistic Gram-negative pathogens of the genus Achromobacter interact with the innate immune system is poorly understood. Using three Achromobacter clinical isolates from two species, we show that the type 3 secretion system (T3SS) is required to induce cell death in human macrophages by inflammasome-dependent pyroptosis. Macrophages deficient in the inflammasome sensors NLRC4 or NLRP3 undergo pyroptosis upon bacterial internalization, but those deficient in both NLRC4 and NLRP3 do not, suggesting either sensor mediates pyroptosis in a T3SS-dependent manner.