The research study revealing that the Escherichia coli’s secreting an weapon; in the launching of some infections. But most of the types of Escherichia coli are harmless; but the ones that are not some they can cause severe life-threatening diarrhea. Worldwide, more than 500,000 children die every year from diarrheal diseases, and pathogenic strains of E. Coli are among the most common causes; according to the World Health Organizations.
These problematic bacteria launch infections by inducing intestinal cells to form tiny structures; called pedestals, that anchor the pathogens in place and help the colonies grow. But the experiments on enteropathogenic and enterohemorrhagic E. Coli showing that when the pathogens were preventing from injecting a protein called EspG into intestinal hosts, the hosts were slower and less effective in producing pedestals that fixed the bacteria in place. Further investigations revealed the cellular pathways hijacking by EspG.
Escherichia coli’s secreting an weapon
But these findings can help by revealing the mechanics of the infection; and suggesting new avenues of treatment. By learning how these pathways work; we think we can develop new ways of interfering with the infection process. But treating these infections can be tricky. Using antibiotics to treat a person with EHEC, for example, can trigger the bacteria to release Shiga toxin, which can lead to a life-threatening infection similar to sepsis.
Researchers have long known that pathogenic E. coli injects its host with a variety of proteins, including EspG. Until now, however, those interactions have been linked only to other biochemical functions. “People had tried to find a link to pedestals before, but they had not finding one. whose work focuses on how bacterial pathogens affect the cytoskeletons of host cells.
The effects of EspG on macrophages
But previously, the researchers studying that the effects of EspG on macrophages; and those findings suggesting that the protein may have an overlooked role in pedestal formation with intestinal hosts. Using fluorescence microscopy, the researchers studied the results. The cells infected by E. Coli lacking EspG took longer to produce pedestals the those by wild-type strains, and what pedestals were produced were shorter.
However, the experiments revealing that the EspG protein hijacks the host cell; by scavenging an active enzyme called PAK. Although previous work has shown a link between EspG and PAK; the new study is the first to connect the two to the formation of pedestals. That connection may help researchers studying other diseases, as well.