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Pseudomonas aeruginosa elastase cleaves a C-terminal peptide from human thrombin that inhibits host inflammatory responses

van Der Plas, Mariena LU ; Bhongir, Ravi LU ; Kjellström, Sven LU ; Siller, Helena; Kasetty, Gopinath LU ; Mörgelin, Matthias LU and Schmidtchen, Artur LU (2016) In Nature Communications 7.
Abstract

Pseudomonas aeruginosa is an opportunistic pathogen known for its immune evasive abilities amongst others by degradation of a large variety of host proteins. Here we show that digestion of thrombin by P. aeruginosa elastase leads to the release of the C-terminal thrombin-derived peptide FYT21, which inhibits pro-inflammatory responses to several pathogen-associated molecular patterns in vitro and in vivo by preventing toll-like receptor dimerization and subsequent activation of down-stream signalling pathways. Thus, P. aeruginosa 'hijacks' an endogenous anti-inflammatory peptide-based mechanism, thereby enabling modulation and circumvention of host responses.

Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
inflammatory responses, Pseudomonas aeruginosa
in
Nature Communications
volume
7
pages
13 pages
publisher
Nature Publishing Group
external identifiers
  • scopus:84968883567
  • wos:000375938800001
ISSN
2041-1723
DOI
10.1038/ncomms11567
language
English
LU publication?
yes
id
f126110c-7c6e-44ef-a75d-4fbf58f0d71d
date added to LUP
2016-06-16 08:53:45
date last changed
2017-04-23 04:51:18
@article{f126110c-7c6e-44ef-a75d-4fbf58f0d71d,
  abstract     = {<p>Pseudomonas aeruginosa is an opportunistic pathogen known for its immune evasive abilities amongst others by degradation of a large variety of host proteins. Here we show that digestion of thrombin by P. aeruginosa elastase leads to the release of the C-terminal thrombin-derived peptide FYT21, which inhibits pro-inflammatory responses to several pathogen-associated molecular patterns in vitro and in vivo by preventing toll-like receptor dimerization and subsequent activation of down-stream signalling pathways. Thus, P. aeruginosa 'hijacks' an endogenous anti-inflammatory peptide-based mechanism, thereby enabling modulation and circumvention of host responses.</p>},
  articleno    = {11567},
  author       = {van Der Plas, Mariena and Bhongir, Ravi and Kjellström, Sven and Siller, Helena and Kasetty, Gopinath and Mörgelin, Matthias and Schmidtchen, Artur},
  issn         = {2041-1723},
  keyword      = {inflammatory responses,Pseudomonas aeruginosa },
  language     = {eng},
  month        = {05},
  pages        = {13},
  publisher    = {Nature Publishing Group},
  series       = {Nature Communications},
  title        = {<i>Pseudomonas aeruginosa</i> elastase cleaves a C-terminal peptide from human thrombin that inhibits host inflammatory responses},
  url          = {http://dx.doi.org/10.1038/ncomms11567},
  volume       = {7},
  year         = {2016},
}