A Pseudomonas aeruginosa TIR effector mediates immune evasion by targeting UBAP1 and TLR adaptors

Details

Serval ID
serval:BIB_BCF5726811CC
Type
Article: article from journal or magazin.
Collection
Publications
Title
A Pseudomonas aeruginosa TIR effector mediates immune evasion by targeting UBAP1 and TLR adaptors
Journal
EMBO J
Author(s)
Imbert P. R., Louche A., Luizet J. B., Grandjean T., Bigot S., Wood T. E., Gagne S., Blanco A., Wunderley L., Terradot L., Woodman P., Garvis S., Filloux A., Guery B., Salcedo S. P.
ISSN
1460-2075 (Electronic)
ISSN-L
0261-4189
Publication state
Published
Issued date
2017
Volume
36
Number
13
Pages
1869-1887
Language
english
Notes
Imbert, Paul Rc
Louche, Arthur
Luizet, Jean-Baptiste
Grandjean, Teddy
Bigot, Sarah
Wood, Thomas E
Gagne, Stephanie
Blanco, Amandine
Wunderley, Lydia
Terradot, Laurent
Woodman, Philip
Garvis, Steve
Filloux, Alain
Guery, Benoit
Salcedo, Suzana P
eng
WT_/Wellcome Trust/United Kingdom
MR/J006874/1/MRC_/Medical Research Council/United Kingdom
MR/K001930/1/MRC_/Medical Research Council/United Kingdom
MR/N023250/1/MRC_/Medical Research Council/United Kingdom
England
EMBO J. 2017 Jul 3;36(13):1869-1887. doi: 10.15252/embj.201695343. Epub 2017 May 8.
Abstract
Bacterial pathogens often subvert the innate immune system to establish a successful infection. The direct inhibition of downstream components of innate immune pathways is particularly well documented but how bacteria interfere with receptor proximal events is far less well understood. Here, we describe a Toll/interleukin 1 receptor (TIR) domain-containing protein (PumA) of the multi-drug resistant Pseudomonas aeruginosa PA7 strain. We found that PumA is essential for virulence and inhibits NF-kappaB, a property transferable to non-PumA strain PA14, suggesting no additional factors are needed for PumA function. The TIR domain is able to interact with the Toll-like receptor (TLR) adaptors TIRAP and MyD88, as well as the ubiquitin-associated protein 1 (UBAP1), a component of the endosomal-sorting complex required for transport I (ESCRT-I). These interactions are not spatially exclusive as we show UBAP1 can associate with MyD88, enhancing its plasma membrane localization. Combined targeting of UBAP1 and TLR adaptors by PumA impedes both cytokine and TLR receptor signalling, highlighting a novel strategy for innate immune evasion.
Keywords
Bacterial Proteins/metabolism, Carrier Proteins/*antagonists & inhibitors, Cell Line, Epithelial Cells/immunology/microbiology, Humans, *Immune Evasion, Membrane Glycoproteins/*antagonists & inhibitors, Myeloid Differentiation Factor 88/*antagonists & inhibitors, Pseudomonas aeruginosa/immunology/*pathogenicity, Receptors, Interleukin-1/*antagonists & inhibitors, Toll-Like Receptors/*antagonists & inhibitors, Virulence Factors/*metabolism, * Pseudomonas, *TIR domain, *TLR adaptors, *ubap1, *virulence
Pubmed
Create date
29/04/2021 10:59
Last modification date
30/04/2021 6:38
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