"Ik denk dat er bij Lyme meer aan de hand is , dat er een soort auto-immuniteit optreedt "
Vanmiddag toen ik op zoek was naar iets anders kwam ik nog een artikel tegen over bacteriële infecties en auto-immune condities. Op pagina 1 (rechts onder) en 2 (links boven) staat er ook een stukje over Borrelia. ( het lukt me niet dat te kopieren) :
Het lukt me nu wel het te kopieren :
Bacterial and viral infections are commonplace in a variety of autoimmune and chronic illnesses such as the chronic fatigue syndrome (myalgic encephalomyelitis), fibromyalgia syndrome, Gulf War illnesses and rheumatoid conditions1-3. Much attention is focused at present on the role of bacteria and the possible mechanisms of their involvement in the pathogenesis of several diseases. The route of infection and penetration and the immune responses of the host can not only make any bacterial infection pathogenic but probably can also determine the aggressiveness of the disease and the chance for full recovery. Therefore the two basic elements addressed here are the association between bacterial infection and autoimmune disease and the involvement of the immune system in the disease process.
Lyme arthritis, which resembles rheumatoid synovial infiltration by Borrelia burgdorferi, has often been suggested to be an autoimmune condition. The B. burgdorferi surface protein A (OspA161-175) is recognised by T-cells and HLA (human leukocyte antigen)-DR molecules that bind this T-cell epitope and to these events is attributed the development of autoimmunity following B. burgdorferi infection. However, these decline with antibiotic therapy16. Therefore, in spite of the perceived association, Drouin et al.17 diligently searched for peptides with sequence homology with OspA (165-173) and have concluded from their study that molecular mimicry might not be significant to pathogenesis. The epitope OspA (163-175) is the predominant epitope associated with Lyme disease. Serum reactivity against OspA is also found in RA patients18. Our knowledge concerning the interaction of B. burgdorferi with host tissues and cells is rather scant. Ghosh et al.19 have suggested cytokeratin 10 as a potential autoantigen. Gavanescu et al.20 reported that mycoplasma infections can result in the production of autoantibodies against centrosomes. It is not known if this cellular organelle is involved with autoimmunity in RA
B. burgdorferi seems to be able to induce inflammatory responses including secretion of cytokines and cellular responses of the T-helper cell-1 (Th-1) type21. Beermann et al.22 generated lipoprotein vesicles (LV) from this bacterium and incorporated them into peripheral blood mononuclear cells. The resultant LV-T cells were predominantly the immune effector CD8+. Furthermore, these cells destroyed autologous T-cells carrying LV. These data do indeed support the existence of an autoimmune condition. Overall, a conservative conclusion would be that the molecular mimicry and autoimmunity thesis is yet to be fully tested
(Edit: gekopieerde tekst toegevoegd)