"Traditional first-line therapy has been based on the belief that the bacteria are bad, so we have to get rid of them as quickly as possible," McCullers said. "But what we are finding is that maybe it is the inflammation we need to worry about first, and the bacteria second. Protein synthesis inhibitors shut down the bacterial protein-making factory, and they can avoid the inflammatory burst by killing them over days instead of quickly lysing them."
In their experiments, the St. Jude researchers infected mice with a mild form of influenza that restricted itself to the lungs. After a week, the scientists infected the mice with pneumonia bacteria. This sequence mimics how humans with influenza would contract secondary pneumonia.
The researchers treated groups of the doubly infected mice with ampicillin, clindamycin, combined clindamycin and ampicillin, or azithromycin. They found that 56 percent of the mice survived with ampicillin treatment, 82 percent survived with clindamycin, 80 percent with clindamycin and ampicillin, and 92 percent with azithromycin. Significantly, while clindamycin and azithromycin both inhibit protein synthesis, azithromycin also has anti-inflammatory properties.
Ampicillin aggravated inflammation compared to clindamycin, the researchers confirmed in test tube studies. The investigators also found evidence of increased inflammation in lung cells of ampicillin-treated animals.
According to McCullers, lung tissue studies of ampicillin-treated animals also revealed the antibiotic's deleterious effects.
"We saw in those animals that, even though we were clearing their lungs of bacteria, the lungs looked just like those of animals in which the bacteria were continuing to multiply
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