A pneumococcal pilus influences virulence and host inflammatory responses
(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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https://lup.lub.lu.se/record/1135194
- author
- organization
- publishing date
- 2006
- 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}}, }