Blockade of IKK signaling induces RIPK1-independent apoptosis in human macrophages.

Regulated cell death in response to microbial infection plays an important role in immune defense and is triggered by pathogen disruption of essential cellular pathways. Gram-negative bacterial pathogens in the Yersinia genus disrupt NF-κB signaling via translocated effectors injected by a type III secretion system, thereby preventing induction of cytokine production and antimicrobial defense. In murine models of infection, Yersinia blockade of NF-κB signaling triggers cell-extrinsic apoptosis through Receptor Interacting Serine-Threonine Protein Kinase 1 (RIPK1) and caspase-8, which is required for bacterial clearance and host survival.

Distinct sequential death complexes regulate pyroptosis and IL-1β release in response to blockade of immune signaling.

Pathogen infection of host cells triggers an inflammatory cell death termed pyroptosis via activation of inflammatory caspases. However, blockade of immune signaling kinases by the virulence factor YopJ triggers cell death involving both apoptotic caspase-8 and pyroptotic caspase-1. While caspase-1 is normally activated within inflammasomes, -induced caspase-1 activation is independent of known inflammasome components.

Collab or Cancel? Bacterial Influencers of Inflammasome Signaling.

The immune system of multicellular organisms protects them from harmful microbes. To establish an infection in the face of host immune responses, pathogens must evolve specific strategies to target immune defense mechanisms. One such defense is the formation of intracellular protein complexes, termed inflammasomes, that are triggered by the detection of microbial components and the disruption of homeostatic processes that occur during bacterial infection.

Salmonella "RecAmends" self-healing.

Persistent bacteria contribute to antibiotic treatment failure, potentially fueling resistance. Persisters must survive host defenses while retaining infective capacity after antibiotic cessation. In this issue of Cell Host and Microbe, Hill et al.