Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2011-8-25
pubmed:abstractText
Lyme neuroborreliosis (LNB) is the most frequent tick-borne infectious disease of the central nervous system. In acute LNB and the rare chronic state of infection, patients can experience cognitive deficits such as attention and memory disturbances. During LNB, single compounds of Borrelia burgdorferi sensu lato are released into the subarachnoid space.To investigate the pathogenesis of neurologic dysfunction in LNB, we determined that the outer surface protein C (OspC), a major virulence factor of B. burgdorferi, stimulated mouse microglial cells in a dose-dependent manner to release nitric oxide (EC50 = 0.24 mg/L) in vitro. To mimic pathophysiologic conditions of long-term release of this bacterial component in vivo, we treated C57BL/6 mice with recombinant OspC from Borrelia garinii or buffer by intraventricular infusion and tested them for behavioral deficits. After 4weeks, brains were examined by routine histology and immunohistochemistry. Assessment of spatial learning and memory of treated mice during OspC exposure did not reveal significant differences from controls. Continuous exposure to intrathecal B. burgdorferi OspC led to activation of microglia and axonal damage without demonstrable cognitive impairment in experimental mice. These results suggest that long-term intrathecal exposure to OspC resulted in axonal damage that may underlie the neurologic manifestations in chronic LNB.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-3069
pubmed:author
pubmed:issnType
Print
pubmed:volume
70
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
748-57
pubmed:meshHeading
pubmed-meshheading:21865883-Animals, pubmed-meshheading:21865883-Animals, Newborn, pubmed-meshheading:21865883-Anti-Bacterial Agents, pubmed-meshheading:21865883-Antigens, Bacterial, pubmed-meshheading:21865883-Antigens, CD, pubmed-meshheading:21865883-Apoptosis, pubmed-meshheading:21865883-Axons, pubmed-meshheading:21865883-Bacterial Outer Membrane Proteins, pubmed-meshheading:21865883-Borrelia burgdorferi, pubmed-meshheading:21865883-Brain, pubmed-meshheading:21865883-Calcium-Binding Proteins, pubmed-meshheading:21865883-Cells, Cultured, pubmed-meshheading:21865883-Chemokine CXCL13, pubmed-meshheading:21865883-Disease Models, Animal, pubmed-meshheading:21865883-Drug Interactions, pubmed-meshheading:21865883-Injections, Spinal, pubmed-meshheading:21865883-Lyme Disease, pubmed-meshheading:21865883-Male, pubmed-meshheading:21865883-Maze Learning, pubmed-meshheading:21865883-Mice, pubmed-meshheading:21865883-Mice, Inbred C57BL, pubmed-meshheading:21865883-Microfilament Proteins, pubmed-meshheading:21865883-Microglia, pubmed-meshheading:21865883-Motor Activity, pubmed-meshheading:21865883-Neurons, pubmed-meshheading:21865883-Polysaccharides, pubmed-meshheading:21865883-Tumor Necrosis Factors, pubmed-meshheading:21865883-Up-Regulation
pubmed:year
2011
pubmed:articleTitle
Long-term intrathecal infusion of outer surface protein C from Borrelia burgdorferi causes axonal damage.
pubmed:affiliation
Department of Neurology (SCT), RWTH Aachen University Hospital, Aachen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't