Findings could lead to better therapies for severe forms of the disease
TUESDAY, July 21 (HealthDay News) -- Researchers at the University of Texas Southwestern Medical Center have figured what genes turn on and off in a person's immune system when he or she has a severe staph infection.
The work, done on children with severe Staphylococcus aureus infections but applicable to all people, could lead to better treatments for these diseases, including the methicillin-resistant (MRSA) version known as the "super bug" because most antibiotics do not work on it.
According to the findings, published in the online journal PLoS One, the genes in children's innate immune system, which provides the most immediate response to infection, became overactive when S. aureus hits. Meanwhile, the genes in the children's adaptive immune systems, which recall past battles to better fight later infections, are shut down.
"It's a very sophisticated and complex dysregulation of the immune system, but our findings prove that there's consistency in the immune response to the staphylococcus bacterium," lead author Monica Ardura, an instructor of pediatrics at UT Southwestern, said in a school news release. "Now that researchers know how the immune system responds, the question is whether this methodology can be used to predict patient outcomes or differentiate the sickest patients from the less sick ones and, ultimately, how this knowledge can be used to develop better therapies?"
She emphasized, though, that the findings were only a snapshot of what occurs during a staph infection at a single moment.
The researchers conducted gene expression profiling with blood taken from 53 otherwise healthy children who had contracted one of the strains of S. aureus during a five-year period and 24 healthy control patients.
The team plans to try to study other conditions surrounding the period before, during and after infection in patients, and how different staph-infection therapies affect treatment.
The Nemours Foundation has more about staph infections.
-- Kevin McKeever
SOURCE: University of Texas Southwestern Medical Center, news release, July 14, 2009
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