Bacterial structure responsible for traveler's diarrhea

For the first time, researchers have deciphered the quasi-atomic structure of filaments, called "pili", which extend from the surface of the bacteria responsible for traveler's diarrhea. Without pili, these bacteria do not cause disease. Knowledge of this structural information can lead to the development of new preventive therapies for the disease.

Traveler's diarrhea is a disadvantage for many people in the United States, but around the world it can be deadly. It causes watery diarrhea that can lead to life-threatening dehydration in infants or other vulnerable populations. With more than one billion cases each year, hundreds of thousands of deaths can be attributed to this bacterial disease caused by Escherichia coli (ETEC), an enterotoxigenic entity, invading the small intestine by pili.

Researchers from the Boston University School of Medicine (BUSM), the University of Virginia, and the University of Umeå have used heat to extract pili from bacteria and then use the electron microscope to examine filaments almost in the native state, frozen in glbad. solid and kept cold using liquid nitrogen. As the pili include hundreds of copies of the same protein, they were able to merge information from many images to determine a high quality three dimensional vision of the filament.

"We anticipate that our new detailed knowledge of the structure of pili will contribute to the development of vaccines and drugs to prevent and treat travelers' diarrhea." We are particularly excited about a peptide found in saliva that can disrupt unwinding and / or rewinding the pili a way to inhibit the adhesion of bacteria and diseases, "explained the corresponding author Esther Bullitt, PhD, badociate professor of physiology and biophysics at BUSM.

These results appear online in the journal of the International Union of Crystallography.

Funding for this study was provided by: the Swedish Research Council (Grant No. 2013-2379 to Magnus Andersson); Kempestiftelserna (grant to Magnus Andersson); National Institutes of Health, National Institute of General Medical Sciences (Grant No. R35GM122510 to Edward Egelman); University of Virginia School of Medicine (Edward Egelman Scholarship); School of Medicine, Boston University (Esther Bullitt Scholarship); National Institutes of Health (Grant No. S10RR025067 and S10-OD018149 to Edward Egelman, Grant No. G20-RR31199 to the University of Virginia).

Source: School of Medicine, Boston University