10.1371/journal.ppat.1003400.g008
Cierra N. Casson
Cierra
N. Casson
Alan M. Copenhaver
Alan
M. Copenhaver
Erin E. Zwack
Erin
E. Zwack
Hieu T. Nguyen
Hieu T.
Nguyen
Till Strowig
Till
Strowig
Bahar Javdan
Bahar
Javdan
William P. Bradley
William
P. Bradley
Thomas C. Fung
Thomas
C. Fung
Richard A. Flavell
Richard
A. Flavell
Igor E. Brodsky
Igor
E. Brodsky
Sunny Shin
Sunny
Shin
Caspase-11 controls multiple pathways of inflammasome activation in response to bacterial secretion systems that access the host cytosol.
Public Library of Science
2013
immunology
Immune cells
monocytes
immunity
Immune activation
Immune defense
Immunity to infections
Innate immunity
microbiology
Bacterial pathogens
Gram negative
inflammation
Host-pathogen interaction
pathogenesis
controls
pathways
inflammasome
activation
bacterial
secretion
systems
2013-06-06 01:04:16
Figure
https://plos.figshare.com/articles/figure/_Caspase_11_controls_multiple_pathways_of_inflammasome_activation_in_response_to_bacterial_secretion_systems_that_access_the_host_cytosol_/713856
<p>Three distinct inflammasome pathways are induced upon interaction of virulent bacteria with host cells. Translocation of flagellin into the host cytosol by specialized secretion systems triggers a NAIP5/NLRC4/caspase-1 inflammasome that leads to cell death, IL-1α, and IL-1β release. Virulent bacteria induce two separate pathways of caspase-11-dependent inflammasome activation through a two-signal model. First, TLR stimulation by PAMPs (signal one) leads to upregulation of pro-IL-1α, pro-IL-1β, NLRP3, and pro-caspase-11. Next, cytosolic detection of virulence activity, namely type III or type IV secretion (signal two), leads to caspase-11 processing and activation. Active caspase-11 contributes to NLRP3-mediated inflammasome activation and caspase-1-dependent IL-1β secretion. Caspase-11 also mediates caspase-1-independent cell death and IL-1α release through a pathway that is independent of the NLRP3/ASC and NAIP5/NLRC4 inflammasomes and involves an unknown host sensor.</p>