Bacteria target immune system cells sent to kill them, study finds
MONDAY, Nov. 12 (HealthDay News) -- Researchers have uncovered a cache of molecular weapons that helps make community-associated methicillin-resistant Staphylococcus aureus (MRSA) so virulent.
Though more work must be done, the study "provides a partial explanation of why these strains are so successful in causing infection and gives a starting point in the development of new drug treatments," said Dr. Gregory Moran, a professor of medicine in the departments of emergency medicine and infectious disease at the Olive View-UCLA Medical Center.
Michael Otto, a senior investigator at the National Institute of Allergy and Infectious Disease, Rocky Mountain Laboratories, and his colleagues searched for and found a battery of short, novel peptides that are expressed by community-associated MRSA strains at higher levels than their hospital-associated MRSA cousins.
Deleting the genes encoding these peptides in mouse models of bacterial infection reduced the microbes' ability to kill or induce skin lesions in infected animals, while purified peptides paralyzed -- and paradoxically, activated -- neutrophils, which are the white blood cells whose job it is to prevent bacterial infections and the principal component of pus.
The study was published in the Nov. 11 online issue of Nature Medicine.
According to the U.S. Centers for Disease Control and Prevention, S. aureus, commonly found on the skin and in the nose of healthy individuals, is associated with bacterial skin infections. MRSA, as its name implies, is a particularly nasty strain of S. aureus that is resistant to the class of antibiotics that includes penicillin, amoxicillin and methicillin.
Traditionally, MRSA, which can cause boils, skin necrosis and even death, has been limited to hospital settings and crowded environments such as prisons. Yet
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