The loss and gain of marginal zone and peritoneal B cells is different in response to relapsing fever and Lyme disease Borrelia.

T cell-independent Abs are protective against Lyme disease and relapsing fever, illnesses caused by Borrelia spirochetes with distinct blood-borne phases of infection. To understand this protective response, we characterized splenic and peritoneal B cell compartments during infection using flow cytometry and immunohistochemistry. In the spleen, early after infection, Borrelia crocidurae, a relapsing fever species, induced a striking loss of marginal zone (MZ) B cells from the MZ, while Borrelia burgdorferi, the agent of Lyme disease, induced the expansion of this subset.

Murine microglia are effective phagocytes for Borrelia burgdorferi.

Lyme disease is a multi-systemic infection that causes diverse neurologic dysfunction collectively known as neuroborreliosis. In the murine model of Lyme disease, Borrelia burgdorferi are seldom found in the nervous system indicating that the spirochetes are rapidly cleared from the brain and peripheral nerves. In the present study, we examined the interaction between microglia and B.

The fur homologue in Borrelia burgdorferi.

Borrelia burgdorferi contains a gene that codes for a Fur homologue. The function of this Fur protein is unknown; however, spirochetes grown at 23 or 35 degrees C expressed fur as determined by reverse transcriptase PCR. The fur gene (BB0647) was cloned and overexpressed as a His-Fur fusion protein in Escherichia coli.

Whole-genome DNA array analysis of the response of Borrelia burgdorferi to a bactericidal monoclonal antibody.

Identification and characterization of genes that contribute to infection with Borrelia burgdorferi and, of those, genes that are targets of host responses is important for understanding the pathogenesis of Lyme disease. The complement-independent bactericidal monoclonal antibody (MAb) CB2 recognizes a carboxy-terminal, hydrophilic epitope of the outer surface protein B (OspB). CB2 kills B.

Astrocytic ceruloplasmin expression, which is induced by IL-1beta and by traumatic brain injury, increases in the absence of the IL-1 type 1 receptor.

IL-1alpha and IL-1beta are induced immediately after insults to the brain, and signaling through the type 1 IL-1 receptor is essential for a normal microglial and astroglial response to injury. To better understand which genes are induced in astrocytes by IL-1beta, we used the unbiased technique of differential display to analyze mouse astroglial gene expression after IL-1beta treatment. Two novel genes were induced, as well as the gene for ceruloplasmin, a ferroxidase with antioxidant properties.