Over two decades ago, a team of researchers at Umeå University in Sweden were pioneers in discovering the mechanism by which Yersinia, a pathogenic bacteria, caused infection in humans. The infection mechanism was found to be a syringe-like protein structure found in the cell walls of the bacteria. The presence of this structure, which was named T3SS (short for Type III secretion system) made it possible for bacterial proteins to be transferred into the cell of the host and subsequently, destroy the metabolism of the host.
In the aftermath of the discovery, it has been observed by researchers that some other species of bacteria also possess T3SS, and T3SS has been established as a common mechanism through which pathogens infect and destroy cells of the host organism. Researchers at Umeå University also pioneered the discovery of the relationship between infection and subsequently, the speedy manufacture of the relevant proteins required to produce the toxic syringe-like protein structure.
The researchers at Umeå university in collaboration with researchers at Helmholtz Centre for Infection Research in Braunschweig, Germany scrutinized the modus operandi of the virulent Yersinia pseudotuberculosis. This bacterium, which is a close relative of the bacterium that was responsible for the deadly plague and bears some similarity with it in its mode of infection, can give rise to vomiting, stomach aches and acute diarrhea. The genes needed by these bacteria for infection can be found on the virulence plasmid, which is an extra circle-shaped chromosome.
Separate infection experiments were carried out in cell cultures using human cells and corroborated with the help of animal models by a team of researchers at The Laboratory for Molecular Infection Medicine Sweden (MIMS) at the Department of Molecular Biology and Umeå Centre for Microbial Research (UCMR). It was discovered that infection could not be induced by a solitary copy of the virulent plasmid. However, it was discovered by the researchers that contact between Yersinia and cells of the host organism set a kind of “copying machine” in motion which multiplied the plasmid population.
Helen Wang, a postdoctoral fellow who conducted majority of the experiments, said Yersinia had evolved a strategy that was considered very brilliant. She further added that since the bacteria required a great deal of energy for it to carry a lot of plasmids, carrying a lot of plasmids would be detrimental to the growth and metabolism of the Yersinia bacteria. But this problem was offset by the brilliant strategy of carrying a single copy of the plasmid which could be quickly multiplied if the need for infection arose. Continuing, Helen Wang said the presence of numerous copies of the plasmids gives bacteria the possibility of accumulating the numerous proteins and T3SS required in order to swiftly overwhelm cells of the host organism in the event of an infection.
Researchers had hitherto been unable to establish that a rise in the population of genes containing plasmids was vital for infection by disease-causing bacteria to be possible.
Tomas Edgren, who led the study alongside Hans Wolf-Watz said the study was a milestone through which they were able to reveal that gene-dosage of genes encoded with plasmids was a smart strategy adopted by bacteria. The discovery will add to our understanding of the mechanism by which bacteria resists antibiotics, and is a step in the right direction in understanding the pathogenic strategy of bacteria.