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Mechanisms of Borrelia burgdorferi Invasion into Tissue

A Medline Search.

Date: February 3, 1999

Inhibition of adherence of Bb to HUVEC by
  • polyclonal antibodies to Bb,
  • monoclonal antibodies to Bb Osp's,
  • fragment antigen binding molecules generated from IgG fraction of rabbit anti-recombinant OspA serum.
Comstock, Fikrig, Shoberg et al.(Winston-Salem) 1993
Bb upregulates E/P-selectin and I/VCAM-1 on mouse EC (brain, joints, heart capillaries) in vitro.
max. after > 50 h incubation time, conc. is dose dependent.
The fact that Bb does not contain conventional LPS suggests that the mode of induction of adhesion molecules on EC is influenced by the phenotype of bacteria.
Boggemeyer, Stehle, Schaible et al. (Freiburg) 1994
Bb upregulates expression of adhesion molecules on EC and promotes NTEM in vitro.
1 Bb per EC stimulates expression of E-selectin (peak at 4 h), VCAM-1 and ICAM-1 (peak at 12 h). NTEM is mediated by E-selectin and CD11/CD18 leukocytic integrins. Depends on dose of spirochetes and length of coincubation period.
Sellati, Burns, Ficazzola, Furie (Stony Brook) 1995
Bb binds human Lys-plasminogen, resulting in enhanced penetration of endothelial monolayers.

Bb possess two binding sites for plasminogen:

  • high-affinity site (106 +/- 14 binding sites/Bb)
    Kd = (24 +/- 12) pM
  • low-affinity site (2,683 +/- 36 binding sites/Bb),
    Kd = (20 +/- 4) nM.
Coleman, Sellati, Testa et al. (Stony Brook) 1995
Binding of human Pgn and uPa to Bb.
Binding of host Pgn and uPa to form a bioactive extracellular matrix protease on Bb could facilitate dissemination and localization of Bb to sites of vascular injury.
Klempner, Noring, Epstein et al. (Boston) 1995
Regulation of chemokine gene expression in HEC and fibroblasts by proinflammatory cytokines and Bb.
Rapid induction of chemokines by inflammatory cytokines and bact. structures (LPS, preparations of Bb), does not require new protein synthesis. Low threshold doses of proinflammatory cytokines -important at the beginning of immune response:
0.1-1 U/ml: MCP-1 and IL-8.
1 U/ml: RANTES, IP-10, mig (synergistic induction). Chemokines might play a central role in the regulation of inflammatory responses and the subsequent immune responses.
Ebnet, Simon, Shaw
(National Cancer Institute, Bethesda)
Bb activates NF-kappa B and is a potent inducer of chemokine and adhesion molecule gene expression in endothelial cells and fibroblasts.
Induction of RANTES, monocyte chemoattractant protein-1, IL-8, GRO-alpha, IP-10 (IFN-inducible protein-10), mig (monokine induced by IFN-gamma), E-selectin, ICAM-1, VCAM-1.
Ebnet, Brown, Siebenlist et al. (National Cancer Institute, Bethesda) 1997
Bb induces chemokines in human monocytes.
IL-8, GRO-alpha, MIP-alpha, MCP-1, RANTES. Rapid and strong Bb-inducible gene expression which was followed by the release of chemokines with peak levels after 12 ... 16 h. Bb itself did not bear or release factors with intrinsic chemotactic activity for monocytes or neutrophils.
Sprenger, Krause, Kaufmann, Priem et al.
Integrins alpha(IIb)beta3, a5b1, alpha(v)beta3 mediate attachment of Bb to human erythroleukemia & saphenous vein EC.
Binding to alpha5bea1, alpha(v)beta3 inhibited by RGD peptides and the appropriate receptor-specific antibodies.
Coburn, Magoun, Bodary, Leong (Boston) 1998
Different classes of proteoglycans contribute to the attachment of Bb to cultured EC and brain cells. Leong, Wang, Magoun et al.

Bb = Borrelia burgdorferi.
EC = endothelial cell.
HEC = human endothelial cells.
HMC = human mononuclear cells.
HPBMC = human peripheral blood mononuclear cells.
HUVEC = human umbellical vein endothelial cells.
NTEM = neutrophil transendothelial migration.
Osp = outer surface (lipo-)proteins of Bb.
Pgn: = plasminogen.
uPa = urokinase-type plasminogen activator.

Further Reading

Smith H, Demonstrating the Intracellularity of Borrelia burgdorferi
Version: April 20, 2001.
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