BB:N SELVIYTYMISMEKANISMEJA

Valvojat: Jatta1001, Borrelioosiyhdistys, Bb

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Bb
Viestit: 1816
Liittynyt: Ma Tammi 26, 2009 23:13

BB:N SELVIYTYMISMEKANISMEJA

Viesti Kirjoittaja Bb » Ke Helmi 11, 2009 19:44

Lähettäjä: Soijuv Lähetetty: 5.10.2004 15:16

Seuraavassa on muutamia tutkimuksia Bb:n kyvystä tuhota esim elimistön lymfosyyttejä jne:


http://www.brown.edu/Courses/Bio_160/Pr ... nesis.html

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David W. Dorward, PhD
Microbiologist, National Institutes of Health, Rocky Mountain Laboratories

In Vitro Evidence for Lymphocytic Membrane Cloaking by Borrelia burgdorferi
David W. Dorward* and Elizabeth R. Fischer. NIH/Rocky Mountain Labs

In vitro studies have demonstrated that Lyme disease spirochetes including Borrelia burgdorferi and B. garinii attach to, invade, and kill subsets of human B and T lymphocytes. To further understand such interactions, temperature-regulated co-incubation mixtures were examined by immunofluorescence and electron microscopy. Low passage (<8 ) B. burgdoferi Sh-2-82 and SKW 6.4 B cells were mixed at 10:1 ratios at 4°C for 1 hr, then warmed to 37°C and followed. Spirochetes attached to nearly 50% of B cells in all mixtures. Whereas, attachment peaked after 1 hr at 37°, invasion appeared to peak at 4 hrs. Addition of 0.1-1% carboxymethycellulose dramatically enhanced the rate of spirochetal motility, but did not increase cell invasion. No evidence for degradation of nor damage to intracellular spirochetes was detected or observed. Emergence form B cells was either lytic or non-lytic. Emergent spirochetes frequently retained lymphocytic membrane envelopes. Video microscopy revealed that enveloped spirochetes had normal motility. After 24 hrs one third of co-incubated spirochetes labeled with antibodies to human B cell antigens. Relatively few spirochetes remained enveloped after 48hrs. Immune electron microscopy showed that although such enveloped spirochetes exhibited surface-exposed B cell antigens, anti-OspA antibodies failed to bind. Furthermore, spirochetes incubated with B cells acquired a time-dependent resistance to classic complement-mediated killing. Such results suggest that in vitro interactions with cultured human B cells result in B. burgdorferi retaining one or more layers of lymphocytic membrane that mask spirochetal antigens, and possible interfere with antibody-mediated recognition and neutralization. If such interactions occur in vivo, such a process could represent a previously unrecognized bacterial virulence strategy. http://www.lyme.org/conferences/98_abstract.html

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Borrelioosin diagnosointi on vaikeaa mm. sen vuoksi että bakteeri kykenee tunkeutumaan mihin tahansa elimeen esim. poskiontelot, iho, silmät, keskushermosto jne. Oireet ovat yksilöllisiä!


Why is it so difficult to diagnose Lyme disease? Borrelia burgdorferi, a bacterial spirochete, causes the condition. This type of bacteria can invade all parts of the body, including skin, muscles, joints, nervous system, the cardiovascular system, ocular tissue, sinus tissue, gastrointestinal tract, and lungs. Lyme disease can also mimic different illnesses and syndromes. It is an infection that triggers a variety of host responses, depending on the individual. The spirochete actually burrows into lymphocyte cells, and exits with the cellular membrane surrounding itself.(1) Thus, it can stimulate an immunological response, including autoimmune mechanisms. Patients with HLA-DR4 and HLA-DR2 genotypes may have genetic predisposition's to chronic Lyme disease.(2) At least one laboratory study reports the IL6-deficient mice have decreased TH2 responses and increased Lyme arthritis.(3) http://www.rhinebeckhealth.com/articles/lyme.htm

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Bb kykenee tuhoamaan lymfosyyttejä!!!


Discussion
Our results indicate that Lyme disease spirochetes can selec-
tively attack and kill purified peripheral human lymphocytes

http://home.pon.net/caat/lyme/killing_lymphocytes.pdf



ATTACKING HUMAN LYMPHOCYTE CELLS

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