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A pneumococcal pilus influences virulence and host inflammatory responses

Barocchi, M A ; Ries, J ; Zogaj, X ; Hemsley, C ; Albiger, Barbara LU ; Kanth, A ; Dahlberg, S ; Fernebro, J ; Moschioni, M and Masignani, V , et al. (2006) In Proceedings of the National Academy of Sciences 103(8). p.2857-2862
Abstract
Streptococcus pneumoniae (pneumococcus) is a major cause of morbidity and mortality world-wide. The initial event in invasive pneumococcal disease is the attachment of encapsulated pneumococci to epithelial cells in the upper respiratory tract. This work provides evidence that initial bacterial adhesion and subsequent ability to cause invasive disease is enhanced by pili, long organelles able to extend beyond the polysaccharide capsule, previously unknown to exist in pneumococci. These adhesive pili-like appendages are encoded by the pneumococcal rlrA islet, present in some, but not all, clinical isolates. Introduction of the rlrA islet into an encapsulated rlrA-negative isolate allowed pilus expression, enhanced adherence to lung... (More)
Streptococcus pneumoniae (pneumococcus) is a major cause of morbidity and mortality world-wide. The initial event in invasive pneumococcal disease is the attachment of encapsulated pneumococci to epithelial cells in the upper respiratory tract. This work provides evidence that initial bacterial adhesion and subsequent ability to cause invasive disease is enhanced by pili, long organelles able to extend beyond the polysaccharide capsule, previously unknown to exist in pneumococci. These adhesive pili-like appendages are encoded by the pneumococcal rlrA islet, present in some, but not all, clinical isolates. Introduction of the rlrA islet into an encapsulated rlrA-negative isolate allowed pilus expression, enhanced adherence to lung epithelial cells, and provided a competitive advantage upon mixed intranasal challenge of mice. Furthermore, a pilus-expressing rlrA islet-positive clinical isolate was more virulent than a nonpiliated deletion mutant, and it out-competed the mutant in murine models of colonization, pneumonia, and bacteremia. Additionally, piliated pneumococci evoked a higher TNF response during systemic infection, compared with nonpiliated derivatives, suggesting that pneumococcal pili not only contribute to adherence and virulence but also stimulate the host inflammatory response. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Proceedings of the National Academy of Sciences
volume
103
issue
8
pages
2857 - 2862
publisher
National Academy of Sciences
external identifiers
  • pmid:16481624
  • scopus:33644526566
ISSN
1091-6490
DOI
10.1073/pnas.0511017103
language
English
LU publication?
yes
id
557f7765-b703-4897-b448-d3a905c55156 (old id 1135194)
date added to LUP
2016-04-01 11:38:32
date last changed
2022-05-06 07:04:38
@article{557f7765-b703-4897-b448-d3a905c55156,
  abstract     = {{Streptococcus pneumoniae (pneumococcus) is a major cause of morbidity and mortality world-wide. The initial event in invasive pneumococcal disease is the attachment of encapsulated pneumococci to epithelial cells in the upper respiratory tract. This work provides evidence that initial bacterial adhesion and subsequent ability to cause invasive disease is enhanced by pili, long organelles able to extend beyond the polysaccharide capsule, previously unknown to exist in pneumococci. These adhesive pili-like appendages are encoded by the pneumococcal rlrA islet, present in some, but not all, clinical isolates. Introduction of the rlrA islet into an encapsulated rlrA-negative isolate allowed pilus expression, enhanced adherence to lung epithelial cells, and provided a competitive advantage upon mixed intranasal challenge of mice. Furthermore, a pilus-expressing rlrA islet-positive clinical isolate was more virulent than a nonpiliated deletion mutant, and it out-competed the mutant in murine models of colonization, pneumonia, and bacteremia. Additionally, piliated pneumococci evoked a higher TNF response during systemic infection, compared with nonpiliated derivatives, suggesting that pneumococcal pili not only contribute to adherence and virulence but also stimulate the host inflammatory response.}},
  author       = {{Barocchi, M A and Ries, J and Zogaj, X and Hemsley, C and Albiger, Barbara and Kanth, A and Dahlberg, S and Fernebro, J and Moschioni, M and Masignani, V and Hultenby, K and Taddei, A R and Beiter, K and Wartha, F and von Euler, A and Covacci, A and Holden, D W and Normark, S and Rappuoli, R and Henriques-Normark, B}},
  issn         = {{1091-6490}},
  language     = {{eng}},
  number       = {{8}},
  pages        = {{2857--2862}},
  publisher    = {{National Academy of Sciences}},
  series       = {{Proceedings of the National Academy of Sciences}},
  title        = {{A pneumococcal pilus influences virulence and host inflammatory responses}},
  url          = {{http://dx.doi.org/10.1073/pnas.0511017103}},
  doi          = {{10.1073/pnas.0511017103}},
  volume       = {{103}},
  year         = {{2006}},
}