Abstract
Francisella tularensis is a gram-negative bacterium and is the causative agent of tularemia – a disease commonly referred to as ‘rabbit fever’. This microbe is extremely virulent as inhalation of fewer than ten bacteria can lead to a lethal infection. During infection, F. tularensis replicates in cells of the immune system, such as macrophages, as well as other non-phagocytes such as epithelial cells and hepatocytes. Moreover, this bacterium has been shown to invade erythrocytes – a process that enhances colonization of ticks (a major disease vector). Our laboratory previously showed that a locus encoding a hypothetical gene, FTL_1228, was induced in the presence of erythrocytes. Therefore, we hypothesized that this gene may be responsible for invasion of these host cells. In this study, we mutated FTL_1228 of F. tularensis LVS. Studies are ongoing to determine the role of this gene in erythrocyte invasion. Preliminary data shows that a strain containing a disruption mutation of FTL_1228 invades erythrocytes at a higher rate than the wild-type F. tularensis LVS. This may suggest that FTL_1228 suppresses red blood cell invasion.
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