The pathophysiology of gut bacterium Streptococcus gallolyticus subsp. gallolyticus (Sgg) remains largely unknown. It is an opportunistic pathogen that has been shown to specifically colonise colorectal cancer tissues via adherence to collagen and, following colonisation, translocation occurs through the intestinal barrier into the bloodstream. Sgg were previously believed to be non-motile.
Microscopy and motility plates show that Sgg are motile bacteria, that may utilise type IV pili for twitching motility. This novel phenotype is abolished in Sgg in response to growth in different carbon sources, but not salt, bile or amino acids. This is not due to an effect on growth, as addition of bile has no effect on motility, but restricts growth. Using western blots we show that Pil1 of Sgg, which is responsible for collagen adherence, is not affected by growth in different sugars. We have confirmed the presence of all essential genes present in the pilus operon by PCR that we propose is required for the observed motility. Overlap extension PCR is currently being used to create knock-out mutants where the ATPase will be deleted and the effect on motility will be established. We show that Sgg adhere to and invade colonic cancer cells. A reduction in invasion is observed when glucose is present. This may correspond to increased cell invasion in cancerous tissues where glucose is limited.
Based on the results from this study, we hypothesise that Sgg regulates motility in response to the metabolic landscape of the human gut to maximise nutrient acquisition, enhance colonisation and ultimately exploit cancer cells resulting in systemic dissemination.