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Tytuł oryginału: Induction of cytokine production in human T cells and monocytes by highly purified lipoteichoic acid: involvement of Toll-like receptors and CD14.
Autorzy: Ellingsen Espen A., Morath Siegfried, Flo Trude H., Schromm Andra B., Hartung Thomas, Thiemermann Christoph, Espevik Terje, Golenbock Douglas T., Foster Simon J., Solberg Rigmor, Aasen Ansgar O., Wang Jacob E.
Źródło: Med. Sci. Monitor 2002: 8 (5) s.BR149-BR156, il., bibliogr. 29 poz.
Sygnatura GBL: 313,278

Hasła klasyfikacyjne GBL:
  • immunologia
  • mikrobiologia
  • farmacja
  • hematologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • in vitro

    Streszczenie angielskie: Pro-inflammatory potential of lipoteichoic acid (LTA) from Staphylococcus aureus is controversial. Present study was undertaken to examine ability of highly purified and characterized S. aureus LTA to stimulate production of pro-inflammatory cytokines in human leukocytes at both mRNA and protein level, and to study involvement of Toll-like receptors (TLRs) adn CD14 in this response. Purified LTA was administered to whole human blood ex-vivo (or primary adherent monocytes) and cytokine response assessed in plasma by EIA. Cytokine mRNA was measured by RT-PCR on leukocyate subsets isolated following stimulation. To study involvement of specific receptors for LTA signaling, CHO cells transfected with CD14 and/or TLR2, TLR4 were used, as well as antibodies directed against these receptors. Addition of highly purified LTA to a whole blood or primary adherent monocytes elicited a time and concentration dependent release of TNF-ŕ, IL-1á, IL-6 and IL-8. mRNA encoding TNF-ŕ, IL-1á, IL-6 and IL-8. mRNA encoding TNF-ŕ, IL-1á and IL-6 seemed to be accumulated in monocytes and T cells, but not in granulocytes and B cells. Expression of TLR2, but not TLR4, in chinese hamster ovary cells conferred responsiveness to LTA. However, antibodies directed towards TLR2 (clone TL2.1) or TLR4 (clone THA125) failed to inhibit TNF-ŕ release induced by LTA in the whole blood model and in adherent monocytes. In contrast, blockade of the CD14 receptor with MAb18D11 strongly attenuated LTA induced release of TNF-ŕ in both models.

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