All Posts Tagged With: "parasitology"

Link: http://www.ncbi.nlm.nih.gov/pubmed/21276171

Excerpt:

Using cryo-electron tomography, we observed closely associated Borrelia cells. Some of these showed a single outer membrane surrounding two longitudinally arranged cytoplasmic cylinders. We also observed fusion of two cytoplasmic cylinders and differences in the surface layer density of fused spirochetes. These processes could play a role in the interaction of Borrelia species with the host’s immune system.

Central Role of the Holliday Junction Helicase RuvAB in vlsE Recombination and Infectivity of Borrelia burgdorferi

Lyme disease is the most prevalent tick-borne infection in North America and Eurasia. It is caused by the bacterium Borrelia burgdorferi and is transmitted to humans via the bite of infected ticks. These spirochetes can cause both acute and chronic infection and inflammation of the skin, joints, heart, and central nervous system. The persistence of infection despite the presence of an active immune response is dependent upon antigenic variation of VlsE, a 35 kDa surface-exposed lipoprotein. A large number of different VlsE variants are present in the host simultaneously and are generated by recombination of the vlsE gene with adjacent vls silent cassettes. To try to identify factors important in vlsE recombination and immune evasion, we selected mutants in genes involved in DNA recombination and repair and screened them for infectivity and vlsE recombination. Mutants in genes encoding RuvA and RuvB (which act together to promote the exchange of strands between two different DNA molecules) had reduced infectivity and greatly diminished vlsE recombination. In immunodeficient mice, ruvA mutants retained full infectivity, and no vlsE recombination was detected. Our findings reinforce the importance of vlsE variation in immune evasion and persistent infection. Continued

Inflammation has long been implicated as a contributor to pathogenesis
in many CNS illnesses, including Lyme neuroborreliosis. Borrelia
burgdorferi is the spirochete that causes Lyme disease and it is known
to potently induce the production of inflammatory mediators in a variety
of cells. In experiments where B. burgdorferi was co-cultured in vitro
with primary microglia, we observed robust expression and release of
IL-6 and IL-8, CCL2 (MCP-1), CCL3 (MIP-1?), CCL4 (MIP-1?) and CCL5
(RANTES), but we detected no induction of microglial apoptosis. In
contrast, SH-SY5Y (SY) neuroblastoma cells co-cultured with B.
burgdorferi expressed negligible amounts of inflammatory mediators and
also remained resistant to apoptosis. Continued