At a Midwestern university, several undergraduates reported to the health service with fever, muscle aches, and vomiting. Blood tests showed they had bacterial food poisoning, caused by Listeria monocytogenes. One student, a biology major, asked how the bacteria were able to get from the intestine into the bloodstream. The physician explained that Listeria cells that express a cell-surface protein, InIA, are able to use receptors on the surface of intestinal cells to gain entry and spread from there to the blood. Once in the blood, the bacteria reach the liver, where they use another cell-surface protein, InIB, to enter liver cells, which are the main sites of infection. She further explained that transcriptional levels of the inIA and inIB genes determine the infective ability of different Listeria strains.
Later, the student discussed this information with her genetics instructor, and together they pondered several questions about how bacteria are able to hijack the normal functions of receptors on human cells as part of their life cycle.
Might these genes be normally expressed at low levels, but undergo increased transcription once in contact with intestinal epithelial cells? How could this be determined?
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