Intestinal fatty acids are exploited by Shigella flexneri to optimize virulence strategies

Pathogenic bacteria are microbes that have virulence genes. These genes give them the ability to make you sick! Virulence genes are also very metabolically expensive-they take a lot of resources to use. So, pathogens need to make a decision: do they use their energy resources to keep dividing and growing, or to cause virulence? 

And how does a little microbe "know" when virulence should be on or off? It can look in its surroundings for signalling molecules-like fatty acids-that can tell it something about location or timing!

Shigella flexneri is a pathogenic bacteria that infects your colon after you ingest it. This microbe causes bacterial dysentery, a severe diarrheal disease. 

S. flexneri's virulence genes lead to abilities like secretion of proteins, spreading between cells, and inflammation-causing mechanisms. When the bacteria decide its time for virulence, it turns on VirF, a protein called a master activator. VirF turns on all other virulence genes. 

When S. flexneri invades your colon, it enters one of the epithelial cells and then travels between them before disupting the layer in a flood of inflammation! The movement between the cells is crucial for virulence, and the gene responsible for cell-to-cell spread is icsA. 

So, if pathogenic bacteria need to use environmental compounds to decide when to turn virulence on/off, then Shigella flexneri must be using compounds in the colon (fatty acids) to control the expression of icsA, a virulence gene controlling cell-to-cell spread!

Based on my plate reader results, I saw repression (less expression) of icsA when all three fatty acid types were present! 

I also saw different levels of repression, like up to a 3 fold reduction in oleic acid, but only up to 1.5 fold in palmitic acid. Why would different fatty acids have different repression levels? Becuase they are different molecules! Different molecules bind differently to proteins like VirF, so they can have greater or less impact on icsA expression.