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Capsule and D-alanylated lipoteichoic acids protect Streptococcus pneumoniae against neutrophil extracellular traps

Wartha, Florian ; Beiter, Katharina ; Albiger, Barbara LU ; Fernebro, Jenny ; Zychlinsky, Arturo ; Normark, Staffan and Henriques-Normark, Birgitta (2007) In Cellular Microbiology 9(5). p.1162-1171
Abstract
Streptococcus pneumoniae is a major cause of morbidity and mortality worldwide. Pneumococci can counteract the action of neutrophils with an antiphagocytic capsule and through electrochemical repulsion of antimicrobial peptides via addition of positive charge to the surface. Pneumococci are captured, but not killed in neutrophil extracellular traps (NETs). Here, we study the role of the polysaccharide capsule and lipoteichoic acid (LTA) modification on pneumococcal interaction with NETs. Expression of capsule (serotypes 1, 2, 4 and 9V) significantly reduced trapping by NETs, but was not required for resistance to NET-mediated killing. Pneumococci contain a dlt operon that mediates the incorporation of d-alanine residues into LTAs, thereby... (More)
Streptococcus pneumoniae is a major cause of morbidity and mortality worldwide. Pneumococci can counteract the action of neutrophils with an antiphagocytic capsule and through electrochemical repulsion of antimicrobial peptides via addition of positive charge to the surface. Pneumococci are captured, but not killed in neutrophil extracellular traps (NETs). Here, we study the role of the polysaccharide capsule and lipoteichoic acid (LTA) modification on pneumococcal interaction with NETs. Expression of capsule (serotypes 1, 2, 4 and 9V) significantly reduced trapping by NETs, but was not required for resistance to NET-mediated killing. Pneumococci contain a dlt operon that mediates the incorporation of d-alanine residues into LTAs, thereby introducing positive charge. Genetic inactivation of dltA in non-encapsulated pneumococci rendered the organism sensitive to killing by antimicrobial components present in NETs. However, the encapsulated dltA mutant remained resistant to NET-mediated killing in vitro. Nevertheless, in a murine model of pneumococcal pneumonia, the encapsulated dltA-mutant strain was outcompeted by the wild-type upon invasion into the lungs and bloodstream. This suggests a non-redundant role for LTA alanylation in pneumococcal virulence at the early stage of invasive disease when capsule expression has been shown to be low. (Less)
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author
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publishing date
type
Contribution to journal
publication status
published
subject
in
Cellular Microbiology
volume
9
issue
5
pages
1162 - 1171
publisher
Wiley-Blackwell
external identifiers
  • pmid:17217430
  • scopus:34047259058
ISSN
1462-5814
DOI
10.1111/j.1462-5822.2006.00857.x
language
English
LU publication?
no
id
169cb2e6-fbb0-4013-bc20-dbfecbdd0e6e (old id 1138117)
date added to LUP
2016-04-01 11:47:18
date last changed
2024-02-23 07:55:31
@article{169cb2e6-fbb0-4013-bc20-dbfecbdd0e6e,
  abstract     = {{Streptococcus pneumoniae is a major cause of morbidity and mortality worldwide. Pneumococci can counteract the action of neutrophils with an antiphagocytic capsule and through electrochemical repulsion of antimicrobial peptides via addition of positive charge to the surface. Pneumococci are captured, but not killed in neutrophil extracellular traps (NETs). Here, we study the role of the polysaccharide capsule and lipoteichoic acid (LTA) modification on pneumococcal interaction with NETs. Expression of capsule (serotypes 1, 2, 4 and 9V) significantly reduced trapping by NETs, but was not required for resistance to NET-mediated killing. Pneumococci contain a dlt operon that mediates the incorporation of d-alanine residues into LTAs, thereby introducing positive charge. Genetic inactivation of dltA in non-encapsulated pneumococci rendered the organism sensitive to killing by antimicrobial components present in NETs. However, the encapsulated dltA mutant remained resistant to NET-mediated killing in vitro. Nevertheless, in a murine model of pneumococcal pneumonia, the encapsulated dltA-mutant strain was outcompeted by the wild-type upon invasion into the lungs and bloodstream. This suggests a non-redundant role for LTA alanylation in pneumococcal virulence at the early stage of invasive disease when capsule expression has been shown to be low.}},
  author       = {{Wartha, Florian and Beiter, Katharina and Albiger, Barbara and Fernebro, Jenny and Zychlinsky, Arturo and Normark, Staffan and Henriques-Normark, Birgitta}},
  issn         = {{1462-5814}},
  language     = {{eng}},
  number       = {{5}},
  pages        = {{1162--1171}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Cellular Microbiology}},
  title        = {{Capsule and D-alanylated lipoteichoic acids protect Streptococcus pneumoniae against neutrophil extracellular traps}},
  url          = {{http://dx.doi.org/10.1111/j.1462-5822.2006.00857.x}},
  doi          = {{10.1111/j.1462-5822.2006.00857.x}},
  volume       = {{9}},
  year         = {{2007}},
}