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Myeloid differentiation factor 88-dependent signalling controls bacterial growth during colonization and systemic pneumococcal disease in mice

Albiger, Barbara LU ; Sandgren, Andreas; Katsuragi, Hiroaki; Meyer-Hoffert, Ulf; Beiter, Katharina; Wartha, Florian; Hornef, Mathias; Normark, Staffan and Normark, Birgitta Henriques (2005) In Cellular Microbiology 7(11). p.1603-1615
Abstract
The Toll-like receptors (TLRs) and the myeloid differentiation factor 88 (MyD88) are key players in the activation of the innate immune defence during microbial infections. Using different murine infection models, we show that MyD88-dependent signalling is crucial for the activation of the innate immune defence against Streptococcus pneumoniae. Our data demonstrate that both local and systemic inflammatory response to S. pneumoniae depends on the presence of MyD88 to clear bacterial colonization of the upper respiratory tract and to prevent pulmonary and systemic infection in mice. Finally, we described a strong correlation between enhanced bacterial growth in the bloodstream of MyD88-deficient mice and the inability to lower the serum... (More)
The Toll-like receptors (TLRs) and the myeloid differentiation factor 88 (MyD88) are key players in the activation of the innate immune defence during microbial infections. Using different murine infection models, we show that MyD88-dependent signalling is crucial for the activation of the innate immune defence against Streptococcus pneumoniae. Our data demonstrate that both local and systemic inflammatory response to S. pneumoniae depends on the presence of MyD88 to clear bacterial colonization of the upper respiratory tract and to prevent pulmonary and systemic infection in mice. Finally, we described a strong correlation between enhanced bacterial growth in the bloodstream of MyD88-deficient mice and the inability to lower the serum iron concentration in response to infection. (Less)
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author
publishing date
type
Contribution to journal
publication status
published
subject
in
Cellular Microbiology
volume
7
issue
11
pages
1603 - 1615
publisher
Wiley-Blackwell
external identifiers
  • pmid:16207247
  • scopus:27244459137
ISSN
1462-5814
DOI
10.1111/j.1462-5822.2005.00578.x
language
English
LU publication?
no
id
2dda3e4e-7cec-41d4-b117-06e6a60bb344 (old id 1132180)
date added to LUP
2008-06-30 13:53:26
date last changed
2017-10-01 03:47:45
@article{2dda3e4e-7cec-41d4-b117-06e6a60bb344,
  abstract     = {The Toll-like receptors (TLRs) and the myeloid differentiation factor 88 (MyD88) are key players in the activation of the innate immune defence during microbial infections. Using different murine infection models, we show that MyD88-dependent signalling is crucial for the activation of the innate immune defence against Streptococcus pneumoniae. Our data demonstrate that both local and systemic inflammatory response to S. pneumoniae depends on the presence of MyD88 to clear bacterial colonization of the upper respiratory tract and to prevent pulmonary and systemic infection in mice. Finally, we described a strong correlation between enhanced bacterial growth in the bloodstream of MyD88-deficient mice and the inability to lower the serum iron concentration in response to infection.},
  author       = {Albiger, Barbara and Sandgren, Andreas and Katsuragi, Hiroaki and Meyer-Hoffert, Ulf and Beiter, Katharina and Wartha, Florian and Hornef, Mathias and Normark, Staffan and Normark, Birgitta Henriques},
  issn         = {1462-5814},
  language     = {eng},
  number       = {11},
  pages        = {1603--1615},
  publisher    = {Wiley-Blackwell},
  series       = {Cellular Microbiology},
  title        = {Myeloid differentiation factor 88-dependent signalling controls bacterial growth during colonization and systemic pneumococcal disease in mice},
  url          = {http://dx.doi.org/10.1111/j.1462-5822.2005.00578.x},
  volume       = {7},
  year         = {2005},
}