[New aspects of the pathogenesis of lyme disease]

Morphological changes of B. burgdorferi as well as changes in expression of surface proteins caused by environmental determinants are essential in pathogenesis of Lyme disease. Cysts, spherical form (spheroplasts, L-form) and "blebs" (gemmae) can be responsible for long lasting antigenic stimulation, signs of chronic borreliosis, and even probably connected with MS and Alzheimer disease. Mechanisms to avoid elimination and persistence in the host include: expression of low heterogenic Osp A, B replaced by polymorphic in sequence and antigenic reactivity OspC, the hindrance of access to some membrane proteins by other proteins on the spirochete's surface, effects of tick saliva proteins action. Hiding of spirochetes is possible by invagination into fibrocytes membrane as well as, coating by antigens derived from lymphocytes B. Distribution of spirochetes is facilitated by binding to platelets through integrin aIIb b3, and to the endothelial cells through integrins av b3 i a5b1, recognition of decorin by lipoproteins DbpA i DbpB, receptor for NAG (N-acetyl glucosamina). Endothelial cells, toxic products of granulocytes, monocytes, macrophages as well as phagocytosis counterpart in pathogenesis. Induced cytokines are connected with activation subsets of T lymphocytes involved in inflammatory response. Cytokines produced by Th1 as cytotoxic CD8 accompany the disease. Important are also dendritic cells regarded as initiators of Th1 response with participation of IL-12. In pathogenesis of Lyme disease participation of autoimmunity is notified, especially molecular similarities between OspA and human lymphocytic antigen (hLFA-1). Neurotoxin, produced by B. burgdorferi Bbtox1 was identified. Encephalopathy signs in Lyme borreliosis could be result of releasing toxico-metabolic products, ability of spirochetes to pass the blood-brain barrier as well as, effect of lymphocytes migration. Active invasion of brain endothelium as ability to adherence to endothelial wall could be the source of focused or disseminated inflammation of brain vessels. Antiaxonal antibodies could disturb axon conduction without damaging. But damage of white matter could be connected with damage of mielin production cells, probably by antibodies, induced in cross reaction.