Enterobacteria, a group of gram-negative bacteria that can thrive in the digestive tract of animals, includes both harmless and pathogenic types of bacteria. Some of the more familiar pathogens within this group of bacteria include Salmonella and E. coli. While it has been clear that these enteropathogenic bacteria prefer the optimal conditions within our gut, the manner in which they establish themselves and proliferate is not well understood. Scientists, in a new article publish in Science, have now discovered that pathogens not only sense their host, but further tailor their gene expression profiles to better infect and colonize their host.
Through what mechanisms do pathogens sense their host and tailor their gene expression profiles?
The pathogens themselves are able to initiate the type III secretion system and related proteins through contact induced expression of NleA. Scientists discovered, through GFP-tagged NleA, that only cells attached to the intestinal wall were able to express the contact-induced version of NleA. Furthermore, it was found that the T3SS mechanism (type III secretion system) was able to inject a group of effector proteins that made the host cell and environment more susceptible to infection. It is through these two key mechanisms caused by the T3SS mechanism that allows enterobacteria to better infect their hosts and cause possible pathogenic effect on their hosts.
|Katsowich et al. Host cell attachment elicits posttranscriptional regulation in infecting enteropathogenic bacteria. Science, 2017; 355 (6326): 735. Neuron, 2017.