Borrelia burgdorferi, the causative agent of Lyme disease, appears during periods of growth to shed membranous material from its surface. Using an antigen capture/detection method developed in the laboratory, this material could be demonstrated on the surface of spirochetes, free in culture medium and in infected animals and ticks. Although the captured antigens were initially assayed by immune electron microscopy, other methods have been used recently to characterize the nature of these bioproducts and to assess their possible role in the pathogenesis of Lyme disease. Researchers in the laboratory have been able to demonstrate that extracellular components of B. burgdorferi 1) appear to be present wherever active growth of the organism is taking place and therefore, may be useful as a diagnostic indicator of active infection and/or treatment effectiveness; 2) are involved in the packaging and protection of intact DNA molecules containing a few known and many unknown genes and gene products; 3) appear to specifically interact with immunoglobulin M molecules in a unique fashion, perhaps to escape immune surveillance; and 4) possesses potent, non-specific mitogenic activity which may cause an inappropriate and noneffective stimulation of the immune system triggering autoimmune disease components. Researchers continue to examine these and other bioproducts with the aim of improving the prevention, treatment and diagnosis of Lyme disease.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Intramural Research (Z01)
Project #
1Z01AI000488-07
Application #
3768807
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
7
Fiscal Year
1993
Total Cost
Indirect Cost
City
State
Country
United States
Zip Code
Carabeo, Reynaldo A; Grieshaber, Scott S; Fischer, Elizabeth et al. (2002) Chlamydia trachomatis induces remodeling of the actin cytoskeleton during attachment and entry into HeLa cells. Infect Immun 70:3793-803
Hoe, Nancy P; Ireland, Robin M; DeLeo, Frank R et al. (2002) Insight into the molecular basis of pathogen abundance: group A Streptococcus inhibitor of complement inhibits bacterial adherence and internalization into human cells. Proc Natl Acad Sci U S A 99:7646-51
Baron, Gerald S; Wehrly, Kathy; Dorward, David W et al. (2002) Conversion of raft associated prion protein to the protease-resistant state requires insertion of PrP-res (PrP(Sc)) into contiguous membranes. EMBO J 21:1031-40
Fields, K A; Fischer, E; Hackstadt, T (2002) Inhibition of fusion of Chlamydia trachomatis inclusions at 32 degrees C correlates with restricted export of IncA. Infect Immun 70:3816-23
Park, H S; Wolfgang, M; van Putten, J P et al. (2001) Structural alterations in a type IV pilus subunit protein result in concurrent defects in multicellular behaviour and adherence to host tissue. Mol Microbiol 42:293-307
Mukhopadhyay, M; Shtrom, S; Rodriguez-Esteban, C et al. (2001) Dickkopf1 is required for embryonic head induction and limb morphogenesis in the mouse. Dev Cell 1:423-34
Zieler, H; Garon, C F; Fischer, E R et al. (2000) A tubular network associated with the brush-border surface of the Aedes aegypti midgut: implications for pathogen transmission by mosquitoes. J Exp Biol 203:1599-611
Carroll, J A; Garon, C F; Schwan, T G (1999) Effects of environmental pH on membrane proteins in Borrelia burgdorferi. Infect Immun 67:3181-7
Garon, C F; Oury, J H; Duran, C M (1999) Virus-like particles in the mitral and tricuspid valves explanted from a patient treated with Fenfluramine-Phentermine. J Heart Valve Dis 8:232