Novel Target For Therapeutics Against Staph Infection
Researchers at the Texas A&M Health Science Center Institute of
Biosciences and Technology, and the University of Edinburgh have
uncovered how a bacterial pathogen interacts with the blood
coagulation protein fibrinogen to cause methicillin-resistant
Staphylococcus aureus (MRSA) infections, a finding that could aid in
developing therapeutics against the potentially deadly disease.
nce occurring more commonly in healthcare facilities, but now
affecting segments of the general population, MRSA is a bacterial
pathogen responsible for a range of diseases from mild skin infection
to life-threatening sepsis. Even with antibiotics, these infections
can still be fatal.
Senior author Magnus Höök, Ph.D. and his colleagues carried out
biochemical and structural studies to determine the binding mechanism
of clumping factor A (ClfA), a surface protein that plays an important
role in the pathogenesis of S. aureus. The group found that ClfA binds
to the blood-clotting protein fibrinogen (Fg) at a site that is also
responsible for inducing platelet activation and thrombosis (clot
inside a blood vessel).
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