Tetraacylated Lipopolysaccharide of Yersinia pestis Can Inhibit Multiple Toll-Like Receptor—Mediated Signaling Pathways in Human Dendritic Cells

Telepnev, Maxim V.; Klimpel, Gary R.; Haithcoat, Judith; Knirel, Yuriy A.; Anisimov, Andrey P.; Motin, Vladimir L.
December 2009
Journal of Infectious Diseases;12/1/2009, Vol. 200 Issue 11, p1694
Academic Journal
Background. Yersinia pestis, the causative agent of plague, showed a temperature-dependent change in lipid A composition, with a reduced degree of acylation when bacteria were grown at 37°C (tetraacylated) versus ambient temperature (hexaacylated). Methods. Human monocytes and monocyte-derived dendritic cells (DCs) were exposed to Y. pestis grown at 26°C or 37°C, to their corresponding lipopolysaccharides (LPS-26°C or LPS-37°C), and to ligands of different Toll-like receptors (TLRs), such as LPS from Escherichia coli (TLR4), lipoprotein (TLR2), polyinosinic-polycytidylic acid (poly-IC) (TLR9), and their combinations. Production of cytokines was measured, along with expression of surface markers of DC maturation. Results. Y. pestis grown at 37°C or LPS-37°C induced much lower production of cytokines (such as tumor necrosis factor a and interleukins 1b, 10, and 12) by DCs than did Y. pestis grown at 26°C or LPS-26°C. Expression of the surface markers HLA-DR, CD86, and CD40 by DCs was also reduced in response to treatment with LPS- 37°C compared with LPS-26°C. Pretreatment of DCs with LPS-37°C inhibited subsequent stimulation with LPS- 26°C, control LPS from E. coli, lipoprotein, or poly-IC. Conclusions. LPS-37°C can inhibit stimulation of DCs not only via TLR4 signaling but also via TLR2 and TLR9.


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