Researchers at the University of Virginia School of Medicine have shown how the common foodborne pathogen Escherichia coli (E. coli) assesses where and when to begin colonizing the human colon. This is through signalling, which signals to the organism that it is in a low-oxygen environment (as with the large intestine). This switches the virulence factor and provides the bacterium with a more effective means for establishing a stronger infection. In essence, E. coli has the capacity to wait until it has reached the-low oxygen large intestine before striking as specific genes are activated.
E. coli is commonly found in the lower intestine of humans and most other warm-blooded animals. Many are harmless; however, some serotypes can cause serious food poisoning in their hosts. Some types of E. coli can cause gastrointestinal infections, as an example (especially as the result of food poisoning). The biggest risk serotypes E. coli produce toxins (Shiga toxins) that can cause severe illness.
Commenting on the new assessment, principal scientists Dr. Melissa Kendall said: “Bacterial pathogens typically colonize a specific tissue in the host. Therefore, as part of their infection strategies, bacterial pathogens precisely time deployment of proteins and toxins to these specific colonization niches in the human host.”
The researcher adds that this mechanism enables the bacteria to conserve energy and hide from being detected by the body’s immune systems. This is known as a virulence factor, which is when a substance released by a microorganism allows it to evade host defences or cause serious injury to the host.
The new research delivers the prospect that through understanding how bacterial pathogens sense where they are in the body, microbiologists may be able to prevent E. coli from sensing where they are inside a human host. This should lead to the organisms passing through the body without causing an infection.
The new research has been published in the journal Proceedings of the National Academy of Sciences. The research paper is titled “The sRNA DicF integrates oxygen sensing to enhance enterohemorrhagic Escherichia coli virulence via distinctive RNA control mechanisms.”
