Bacterial outer membrane vesicles and host cell death signaling

The programmed cell death pathways of pyroptosis and apoptosis protect mammals from infections. The activation of host cell death signaling depends on cell surface and cytosolic receptors that bind bacterial molecules or sense their activity. The formation of cytosolic protein complexes, such as the inflammasome and apoptosome, activates caspases, pore-forming proteins, and inflammatory cytokines. These pathways respond to bacteria and their released membrane vesicles. Outer membrane vesicles (OMVs) that emerge from the outer membrane of Gram-negative bacteria deliver a range of bacterial molecules, including lipids, proteins, polysaccharides and nucleic acids to host cells. Recent findings describe how OMV-associated molecules activate pyroptosis, apoptosis, and other inflammatory pathways. We discuss here how OMV-associated molecules are sensed by the immune system and how this contributes to infections and inflammatory diseases.

Automated summary

The programmed cell death pathways of pyroptosis and apoptosis protect mammals from infections by activating host cell death signaling that depends on cell surface and cytosolic receptors binding bacterial molecules or sensing their activity. Outer membrane vesicles (OMVs) released from Gram-negative bacteria deliver bacterial molecules to host cells, activating pyroptosis, apoptosis, and other inflammatory pathways.