Antibiotics could help a drug-resistant pathogen to worsen inflammation.
Methicillin-resistant Staphylococcus aureus (MRSA) resists most β-lactam antibiotics by acquiring a protein that modifies the cell wall. David Underhill, George Liu and their team at Cedars-Sinai Medical Center in Los Angeles, California, thought that this modification might also boost the production of inflammatory molecules called cytokines in the host. They exposed mouse and human immune cells to MRSA and found that the host cells made higher levels of a cytokine called IL-1β when MRSA had been grown in the presence of β-lactams. In mice, treatment with a β-lactam caused more immune cells to flood the site of an MRSA skin infection, resulting in more inflammation and larger abscesses than in MRSA-infected mice that were not treated with the antibiotic.
MRSA infections are still sometimes treated with β-lactams, but these should be used with other antibiotic classes, the authors write.