1887

Abstract

causes neonatal meningitis frequently complicated with multiple brain abscesses. During central nervous system infection in the neonatal rat model, previous studies have documented many bacteria-filled macrophages within the neonatal rat brain and abscesses. Previous studies have also shown that is taken up by, survives phagolysosomal fusion and replicates in macrophages and . In this study, in order to elucidate genetic and cellular factors contributing to persistence, a combinatory technique of differential fluorescence induction and transposon mutagenesis was employed to isolate genes induced while inside macrophages. Several banks of mutants were subjected to a series of enrichments to select for  : : transposon fusion into genes that are turned off but expressed when intracellular within macrophages. Further screening identified several mutants attenuated in their recovery from macrophages compared with the wild-type. A mutation within an homologue caused significant attenuation in uptake and hypervirulence , resulting in death within 24 h. Furthermore, analysis of the immunoregulatory interleukin (IL)-10/IL-12 cytokine response during infection suggested that expression may alter this response. A better understanding of the bacteria–macrophage interaction at the molecular level and its contribution to brain abscess formation will assist in developing preventative and therapeutic strategies.

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2006-12-01
2024-04-19
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