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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
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Disease relevance of Spirochaetales


Psychiatry related information on Spirochaetales


High impact information on Spirochaetales

  • PLG was not detected in spirochetes from unfed ticks, but binding occurred as ticks fed on the host's blood [7].
  • Acetogenesis from H2 plus CO2 by spirochetes from termite guts [8].
  • Mice given both P35 and P37 antisera were protected from challenge with 10(2) B. burgdorferi, and P35 and P37 antisera also afforded protection when administered 24 hr after spirochete challenge [9].
  • They are unique among invasive spirochetes in that they contain outer membrane lipopolysaccharide (LPS) as well as lipoproteins [10].
  • In immunocompetent mice, spirochetes that did not express ospC (the outer-surface protein C gene) were selected within 17 d after inoculation, concomitantly with the emergence of anti-OspC antibody [11].

Chemical compound and disease context of Spirochaetales

  • Moreover, results from three independent methodologies, i.e., (a) indirect immunofluorescence analysis of agarose-encapsulated organisms, (b) proteinase K treatment of intact spirochetes, and (c) Triton X-114 phase partitioning of T. pallidum conclusively demonstrated that native TprK is entirely periplasmic [12].
  • Accordingly, we determined whether antigenically variable spirochetes delivered by naturally infected ticks, collected from a site where transmission is intense, may fail to infect mice actively immunized with recombinant glutathione transferase outer surface fusion proteins A or B (OspA and OspB) [13].
  • Subcutaneous inoculation of 10(4) spirochetes resulted in a peak spirochetemia five days after infection with 20-23 x 10(6) organisms per milliliter of whole blood in all mice, indicating that the PAS had no effect on the development of this phase of the infection [14].
  • The spirochetes were eliminated upon treatment with neomycin and bacitracin, but the symptoms of the patients remained unchanged [15].
  • This contrasted with the intense fluorescence observed when encapsulated spirochetes were probed in the presence of 0.06% Triton X-100, which selectively removed outer membranes [16].

Biological context of Spirochaetales

  • This is, to our knowledge, the first description of the targeted disruption of a candidate B. burgdorferi virulence factor with a known biochemical function that can be quantified, and demonstrates the importance of B. burgdorferi P66 in the attachment of this pathogenic spirochete to a human cell-surface receptor [17].
  • The results indicate that asymmetrical rotation of the flagellar bundles of spirochetes does not depend upon the chemotaxis system but rather upon differences between the two flagellar bundles [3].
  • Vsp surface lipoproteins are serotype-defining antigens of relapsing fever spirochetes that undergo multiphasic antigenic variation to avoid the immune response [18].
  • Coiling phagocytosis discriminates between different spirochetes and is enhanced by phorbol myristate acetate and granulocyte-macrophage colony-stimulating factor [19].
  • Consistent with this, the spirochete bound to immobilized heparin, and soluble heparin inhibited bacterial adhesion to mammalian cells [20].

Anatomical context of Spirochaetales


Gene context of Spirochaetales

  • IL-1 beta synthesis increased in response to increasing numbers of spirochetes, whereas IL-1ra synthesis did not [2].
  • These studies indicate opposing roles for IL-4 and IFN-gamma in the modulation of spirochete growth and disease development in B. burgdorferi-infected mice and suggest that differential cytokine production early in infection may contribute to strain-related differences in susceptibility [25].
  • Overall, these data indicated that the p38 MAP kinase pathway plays an important role in B. burgdorferi-elicited inflammation and point to potential new therapeutic approaches to the treatment of inflammation induced by the spirochete [26].
  • The results are consistent with a major role played by IL-10 in controlling the initial phase of infection with this spirochete [27].
  • No TNF-alpha or IL-1beta were produced by LN cells from infected mice of either strain in response to lipoprotein or B. burgdorferi spirochetes [28].

Analytical, diagnostic and therapeutic context of Spirochaetales


  1. Fibronectin tetrapeptide is target for syphilis spirochete cytadherence. Thomas, D.D., Baseman, J.B., Alderete, J.F. J. Exp. Med. (1985) [Pubmed]
  2. Live Borrelia burgdorferi preferentially activate interleukin-1 beta gene expression and protein synthesis over the interleukin-1 receptor antagonist. Miller, L.C., Isa, S., Vannier, E., Georgilis, K., Steere, A.C., Dinarello, C.A. J. Clin. Invest. (1992) [Pubmed]
  3. Asymmetrical flagellar rotation in Borrelia burgdorferi nonchemotactic mutants. Li, C., Bakker, R.G., Motaleb, M.A., Sartakova, M.L., Cabello, F.C., Charon, N.W. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  4. Bell's palsy and secondary syphilis: CSF spirochetes detected by immunofluorescence. Davis, L.E., Sperry, S. Ann. Neurol. (1978) [Pubmed]
  5. Purification and substrate specificity of an endopeptidase from the human oral spirochete Treponema denticola ATCC 35405, active on furylacryloyl-Leu-Gly-Pro-Ala and bradykinin. Mäkinen, K.K., Mäkinen, P.L., Syed, S.A. J. Biol. Chem. (1992) [Pubmed]
  6. Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease. Miklossy, J., Khalili, K., Gern, L., Ericson, R.L., Darekar, P., Bolle, L., Hurlimann, J., Paster, B.J. J. Alzheimers Dis. (2004) [Pubmed]
  7. Plasminogen is required for efficient dissemination of B. burgdorferi in ticks and for enhancement of spirochetemia in mice. Coleman, J.L., Gebbia, J.A., Piesman, J., Degen, J.L., Bugge, T.H., Benach, J.L. Cell (1997) [Pubmed]
  8. Acetogenesis from H2 plus CO2 by spirochetes from termite guts. Leadbetter, J.R., Schmidt, T.M., Graber, J.R., Breznak, J.A. Science (1999) [Pubmed]
  9. Borrelia burgdorferi P35 and P37 proteins, expressed in vivo, elicit protective immunity. Fikrig, E., Barthold, S.W., Sun, W., Feng, W., Telford, S.R., Flavell, R.A. Immunity (1997) [Pubmed]
  10. Leptospiral lipopolysaccharide activates cells through a TLR2-dependent mechanism. Werts, C., Tapping, R.I., Mathison, J.C., Chuang, T.H., Kravchenko, V., Saint Girons, I., Haake, D.A., Godowski, P.J., Hayashi, F., Ozinsky, A., Underhill, D.M., Kirschning, C.J., Wagner, H., Aderem, A., Tobias, P.S., Ulevitch, R.J. Nat. Immunol. (2001) [Pubmed]
  11. An immune evasion mechanism for spirochetal persistence in Lyme borreliosis. Liang, F.T., Jacobs, M.B., Bowers, L.C., Philipp, M.T. J. Exp. Med. (2002) [Pubmed]
  12. The TprK protein of Treponema pallidum is periplasmic and is not a target of opsonic antibody or protective immunity. Hazlett, K.R., Sellati, T.J., Nguyen, T.T., Cox, D.L., Clawson, M.L., Caimano, M.J., Radolf, J.D. J. Exp. Med. (2001) [Pubmed]
  13. Protection against antigenically variable Borrelia burgdorferi conferred by recombinant vaccines. Telford, S.R., Fikrig, E., Barthold, S.W., Brunet, L.R., Spielman, A., Flavell, R.A. J. Exp. Med. (1993) [Pubmed]
  14. The plasminogen activation system enhances brain and heart invasion in murine relapsing fever borreliosis. Gebbia, J.A., Monco, J.C., Degen, J.L., Bugge, T.H., Benach, J.L. J. Clin. Invest. (1999) [Pubmed]
  15. Colorectal spirochetosis: clinical significance of the infestation. Nielsen, R.H., Orholm, M., Pedersen, J.O., Hovind-Hougen, K., Teglbjaerg, P.S., Thaysen, E.H. Gastroenterology (1983) [Pubmed]
  16. Limited surface exposure of Borrelia burgdorferi outer surface lipoproteins. Cox, D.L., Akins, D.R., Bourell, K.W., Lahdenne, P., Norgard, M.V., Radolf, J.D. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  17. Targeted mutation of the outer membrane protein P66 disrupts attachment of the Lyme disease agent, Borrelia burgdorferi, to integrin alphavbeta3. Coburn, J., Cugini, C. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  18. Structural conservation of neurotropism-associated VspA within the variable Borrelia Vsp-OspC lipoprotein family. Zuckert, W.R., Kerentseva, T.A., Lawson, C.L., Barbour, A.G. J. Biol. Chem. (2001) [Pubmed]
  19. Coiling phagocytosis discriminates between different spirochetes and is enhanced by phorbol myristate acetate and granulocyte-macrophage colony-stimulating factor. Rittig, M.G., Jagoda, J.C., Wilske, B., Murgia, R., Cinco, M., Repp, R., Burmester, G.R., Krause, A. Infect. Immun. (1998) [Pubmed]
  20. Hemagglutination and proteoglycan binding by the Lyme disease spirochete, Borrelia burgdorferi. Leong, J.M., Morrissey, P.E., Ortega-Barria, E., Pereira, M.E., Coburn, J. Infect. Immun. (1995) [Pubmed]
  21. Toll-like receptor 2 is required for innate, but not acquired, host defense to Borrelia burgdorferi. Wooten, R.M., Ma, Y., Yoder, R.A., Brown, J.P., Weis, J.H., Zachary, J.F., Kirschning, C.J., Weis, J.J. J. Immunol. (2002) [Pubmed]
  22. Lyme arthritis synovial gamma delta T cells respond to Borrelia burgdorferi lipoproteins and lipidated hexapeptides. Vincent, M.S., Roessner, K., Sellati, T., Huston, C.D., Sigal, L.H., Behar, S.M., Radolf, J.D., Budd, R.C. J. Immunol. (1998) [Pubmed]
  23. Characterization of the physiological requirements for the bactericidal effects of a monoclonal antibody to OspB of Borrelia burgdorferi by confocal microscopy. Escudero, R., Halluska, M.L., Backenson, P.B., Coleman, J.L., Benach, J.L. Infect. Immun. (1997) [Pubmed]
  24. Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro. Georgilis, K., Peacocke, M., Klempner, M.S. J. Infect. Dis. (1992) [Pubmed]
  25. Role of IL-4 and IFN-gamma in modulation of immunity to Borrelia burgdorferi in mice. Keane-Myers, A., Nickell, S.P. J. Immunol. (1995) [Pubmed]
  26. Murine Lyme arthritis development mediated by p38 mitogen-activated protein kinase activity. Anguita, J., Barthold, S.W., Persinski, R., Hedrick, M.N., Huy, C.A., Davis, R.J., Flavell, R.A., Fikrig, E. J. Immunol. (2002) [Pubmed]
  27. Interleukin-10 modulates proinflammatory cytokines in the human monocytic cell line THP-1 stimulated with Borrelia burgdorferi lipoproteins. Murthy, P.K., Dennis, V.A., Lasater, B.L., Philipp, M.T. Infect. Immun. (2000) [Pubmed]
  28. Differential acquired immune responsiveness to bacterial lipoproteins in Lyme disease-resistant and -susceptible mouse strains. Ganapamo, F., Dennis, V.A., Philipp, M.T. Eur. J. Immunol. (2003) [Pubmed]
  29. Direct demonstration of antigenic substitution of Borrelia burgdorferi ex vivo: exploration of the paradox of the early immune response to outer surface proteins A and C in Lyme disease. Montgomery, R.R., Malawista, S.E., Feen, K.J., Bockenstedt, L.K. J. Exp. Med. (1996) [Pubmed]
  30. Characterization of VspB of Borrelia turicatae, a major outer membrane protein expressed in blood and tissues of mice. Pennington, P.M., Cadavid, D., Barbour, A.G. Infect. Immun. (1999) [Pubmed]
  31. Production of interleukin-8 (IL-8) by cultured endothelial cells in response to Borrelia burgdorferi occurs independently of secreted [corrected] IL-1 and tumor necrosis factor alpha and is required for subsequent transendothelial migration of neutrophils. Burns, M.J., Sellati, T.J., Teng, E.I., Furie, M.B. Infect. Immun. (1997) [Pubmed]
  32. Borrelia burgdorferi induces the production and release of proinflammatory cytokines in canine synovial explant cultures. Straubinger, R.K., Straubinger, A.F., Summers, B.A., Erb, H.N., Härter, L., Appel, M.J. Infect. Immun. (1998) [Pubmed]
  33. Specificity of infection-induced immunity among Borrelia burgdorferi sensu lato species. Barthold, S.W. Infect. Immun. (1999) [Pubmed]
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