Fibers known to be important in Alzheimers disease also are produced by bacteria that cause ailments such as urinary tract infections, according to research at Washington University School of Medicine in St. Louis. The finding is described in the February 1 issue of the journal Science.
Scott J. Hultgren, Ph.D., the Helen Lehbrink Stoever Professor of Molecular Microbiology, led the study; Matthew R. Chapman, Ph.D., post-doctoral fellow in molecular microbiology was first author.
The scientists found that certain strains of the bacterium Escherichia coli (E. coli) produce amyloid fibers similar to those that can accumulate in the brain to form senile plaques, a hallmark of Alzheimers disease. The bacterial fibers, known as curli, form a meshwork around the bacteria, joining them together in clusters or communities known as biofilms. Bacteria in biofilms are more resistant to antibiotics and to the bodys immune defenses.
The discovery marks the first time that amyloid has been found in bacteria. Previously, amyloid was thought to be made only by cells of higher organisms. Even then, their presence was regarded as a mistake, a biological error.
This is the first example of a dedicated molecular machinery to produce amyloid and thus shows that amyloid production is not always a mistake, says Hultgren. This finding gives us a powerful genetic system to study the molecular details of amyloid formation and may allow us to begin designing drugs that will block the formation of amyloid or treat or prevent human amyloid diseases.
Salmonella bacteria also produce bacterial amyloid or curli, and the genes for curli production exist in other bacteria, as well, says Chapman.
The process of curli production is similar to the formation of a snowflake on a dust particle. The particle is a nucleus that triggers the precipitation of ice crystals at its surface, setting off a chain reaction that leads to more ice crystals and gro
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Contact: Darrell E. Ward
wardd@msnotes.wustl.edu
314-286-0122
Washington University School of Medicine
31-Jan-2002