Protein on surface of MRSA plays key role in infecting
14 July 2010
An international research team has identified a protein that
plays a key roll in enabling the MRSA bacteria to infect human cells.
Staphylococcus aureus is a type of bacteria commonly
found on the skin that is relatively harmless unless it gets into
the bloodstream, where it can cause blood poisoning and create
abscesses in organs such as the heart and brain.
MRSA, or methicillin resistant Staphylococcus aureus,
can be particularly dangerous because it is resistant to treatment
with most antibiotics.
Researchers at the University of Bath, in collaboration with the
Universities of York and Gothenburg, investigated how the bug moves
from the bloodstream to invade organs in the body.
They studied Fibronectin Binding Protein (FnBP), a protein on the
surface of the bacterium that enables it to bind to human cells and
The Wellcome Trust-funded study, published in the open access
journal PLoS Pathogens, proved for the first time this protein is
central to the bacteria’s ability to invade the organs. The next
step of their research will be to try and stop the bacteria invading
human cells by using antibodies to block FnBP binding.
Dr Andrew Edwards, a postdoctoral researcher from the University
of Bath’s Department of Biology & Biochemistry, explained: “The 3D
shape of FnBP interested us because it contains a portion that’s
repeated lots of times in the overall structure. We wanted to find
out why it needs so many repeats.
“We found that although only one repeat was needed to bind to
cells, altering the protein to contain a smaller number of repeats
reduced the strength of binding and resulted in a less severe
Dr Ruth Massey, Senior Lecturer from the University of Bath’s
Department of Biology & Biochemistry, added: “If we can develop a
treatment that blocks the binding of FnBP to cells, it could help
stop the infection spreading to the major organs in the body.
“Whilst such a treatment wouldn’t kill the bacteria, it could be
used in parallel with antibiotics to stop the infection becoming
more dangerous and spreading to the patient’s organs.”
The researchers will spend the next three years working to block
FnBP binding, and predict that a treatment for patients could be
developed in as little as a decade.