Host immunity and cellular responses to bacterial outer membrane vesicles

All Gram-negative bacteria secrete outer membrane vesicles (OMVs) that contain components of the bacterial outer membrane, including lipopolysaccharide and outer membrane proteins. Bacteria use OMVs to deliver toxins into host cells that can modulate host cell homeostasis and induce cytopathic effects. Epithelial cells and myeloid cells recognize pathogen-associated molecular patterns (PAMPs) present in OMVs and trigger innate immune signaling leading to the secretion of proinflammatory cytokines. OMVs can also trigger adaptive immune responses by activating T and B cells. All Gram-negative bacteria produce outer membrane vesicles (OMVs) which are minute spherical structures emanating from the bacterial outer membrane. OMVs are primarily enriched in lipopolysaccharide (LPS) and phospholipids, as well as outer membrane and periplasmic proteins. Recent research has provided convincing evidence for their role in multiple aspects of bacterial physiology and their interaction with vertebrate host cells. OMVs play vital roles in bacterial colonization, delivery of virulence factors, and disease pathogenesis. Here, we discuss the interactions of OMVs with mammalian host cells with a focus on how bacteria use OMVs to modulate host immune responses that eventually enable bacteria to evade host immunity. All Gram-negative bacteria produce outer membrane vesicles (OMVs) which are minute spherical structures emanating from the bacterial outer membrane. OMVs are primarily enriched in lipopolysaccharide (LPS) and phospholipids, as well as outer membrane and periplasmic proteins. Recent research has provided convincing evidence for their role in multiple aspects of bacterial physiology and their interaction with vertebrate host cells. OMVs play vital roles in bacterial colonization, delivery of virulence factors, and disease pathogenesis. Here, we discuss the interactions of OMVs with mammalian host cells with a focus on how bacteria use OMVs to modulate host immune responses that eventually enable bacteria to evade host immunity. cell entry mechanism mediated by intracellular adaptor proteins clathrin and caveolin. molecules that act as ‘danger’ signals for host cells and can initiate immune signaling cascades to counter DAMPs. condition in which bacteria produce high amounts of membrane vesicles. multiprotein complex that serves as an intracellular ‘receptor’ recognizing intracellular DAMPs and initiating innate immune signaling. cell entry mechanism mediated by cholesterol and sphingolipid-rich plasma membrane domains called ‘lipid rafts.’ nonselective cell entry mechanism mediated by the actin cytoskeleton. intracellular PRR that belongs to the family of NOD-like receptors, and functions by detecting intracellular PAMPs, and subsequently activates immune signaling. germline-encoded host cell receptors that can recognize PAMPs to mount immune responses. highly inflammatory form of lytic cell death; often induced upon pathogenic infections. biological process that enables bacterial cell-to-cell communication, regulating bacterial gene expression in response to bacterial cell density. a subpopulation of CD4+ helper T cells whose function is to suppress immune responses and thus maintain homeostasis and tolerance. class of antigen that induces an excessively strong immune response that triggers CD4+ T cells by binding directly to MHC class II molecules (independently from the classic binding via the highly variable T cell receptor peptide groove); generally derived from Streptococcus or Staphylococcus species. proinflammatory response initiated by CD4+ helper Th2 and Th17 cells in which IL-4, IL-5, IL-13, and IL-17 cytokines are secreted to activate B cells and recruit other immune cells to sites of infection. class of host pathogen recognition receptors that initiate innate immune signaling upon recognition of conserved pathogen-associated molecular patterns.