Toll-like receptor 9 acts at an early stage in host defence against pneumococcal infection

Barbara Albiger, Sofia Dahlberg, Andreas Sandgren, Florian Wartha, Katharina Beiter, Hiroaki Katsuragi, Shizuo Akira, Staffan Normark, Birgitta Henriques-Normark

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskriftPeer review

Sammanfattning

Toll-like receptor 9 (TLR9) induces an inflammatory response by recognition of unmethylated CpG dinucleotides, mainly present in prokaryotic DNA. So far, TLR9-deficient mice have been shown to be more sensitive than wild-type mice to viral, but not to bacterial infections. Here, we show that mice deficient in TLR9 but not in TLR1, TLR2, TLR4 and TLR6 or IL-1R/IL-18R are more susceptible to a respiratory tract bacterial infection caused by Streptococcus pneumoniae. Intranasal challenge studies revealed that TLR9 plays a protective role in the lungs at an early stage of infection prior to the entry of circulating inflammatory cells. Alveolar as well as bone marrow-derived macrophages deficient in either TLR9 or the myeloid adaptor differentiation protein MyD88 were impaired in pneumococcal uptake and in pneumococcal killing. Our data suggest that in the airways, pneumococcal infection triggers a TLR9 and MyD88-dependent activation of phagocytic activity from resident macrophages leading to an early clearance of bacteria from the lower respiratory tract.
Originalspråkengelska
Sidor (från-till)633-644
TidskriftCellular Microbiology
Volym9
Nummer3
DOI
StatusPublished - 2007
Externt publiceradJa

Ämnesklassifikation (UKÄ)

  • Mikrobiologi

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