Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10940833 | Immunobiology | 2015 | 10 Pages |
Abstract
Borrelia burgdorferi can be categorized based on restriction fragment length polymorphism analysis into ribosomal spacer type (RST) 1, 2 and 3. A correlation between RST type and invasiveness of Borrelia isolates has been demonstrated in clinical studies and experimental models, and RST 1 isolates are more likely to cause disseminated disease than RST 3 isolates. We hypothesized that this could partially be due to increased susceptibility of RST 3 isolates to killing by the innate immune system early in infection. Thus, we investigated the interaction of five RST 1 and five RST 3 isolates with various components of the human innate immune system in vitro. RST 3 isolates induced significantly greater upregulation of activation markers in monocyte-derived dendritic cells compared to RST 1 isolates at a low multiplicity of infection. However, RST 1 isolates stimulated greater interleukin-6 production. At a high multiplicity of infection no differences in dendritic cell activation or cytokine production were observed. In addition, we observed no differences in the ability of RST 1 and RST 3 isolates to activate monocytes or neutrophils and all strains were phagocytosed at a comparable rate. Finally, all isolates tested were equally resistant to complement-mediated killing, as determined by dark-field microscopy and a growth inhibition assay. In conclusion, we demonstrate that the RST 1 and 3 isolates showed no distinction in their susceptibility to the various components of the human immune system studied here, suggesting that other factors are responsible for their differential invasiveness.
Keywords
HLA-DRTNFOuter surface protein CCytokine bead arrayospChuman leukocyte antigen-DRCFSEMoDCNHSRSTCBALPSPBMCMFIMOIErythema migransInnate immunityinterferonIFNinterleukinBorreliaHIScluster of differentiationnormal human serumPeripheral blood mononuclear cellDendritic cellMonocyte-derived dendritic celltumour necrosis factorLymelipopolysaccharideMACmean fluorescence intensityLinear plasmidmembrane attack complexmultiplicity of infection
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Authors
Lauren M.K. Mason, Eduard A. Herkes, Michelle A. Krupna-Gaylord, Anneke Oei, Tom van der Poll, Gary P. Wormser, Ira Schwartz, Mary M. Petzke, Joppe W.R. Hovius,