TY - JOUR
T1 - Bacterial outer membrane vesicles and host cell death signaling
AU - Dhital, Subhash
AU - Deo, Pankaj
AU - Stuart, Isabella
AU - Naderer, Thomas
N1 - Funding Information:
We were unable to reference all relevant work due to space constraints. Figures were generated in BioRender. Our laboratory is supported by grants from the National Health and Medical Research Council ( 1183848 , 1163556 ). T.N. is an Australian Research Council Future Fellow ( FT170100313 ).
Funding Information:
We were unable to reference all relevant work due to space constraints. Figures were generated in BioRender. Our laboratory is supported by grants from the National Health and Medical Research Council (1183848, 1163556). T.N. is an Australian Research Council Future Fellow (FT170100313). There are no interests to declare.
Publisher Copyright:
© 2021 Elsevier Ltd
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2021/12
Y1 - 2021/12
N2 - 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.
AB - 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.
KW - apoptosis
KW - inflammasome
KW - inflammation
KW - macrophage
KW - OMV
KW - pyroptosis
UR - http://www.scopus.com/inward/record.url?scp=85105777279&partnerID=8YFLogxK
U2 - 10.1016/j.tim.2021.04.003
DO - 10.1016/j.tim.2021.04.003
M3 - Review Article
AN - SCOPUS:85105777279
SN - 0966-842X
VL - 29
SP - 1106
EP - 1116
JO - Trends in Microbiology
JF - Trends in Microbiology
IS - 12
ER -