Dexamethasone Affects the Neutrophil-Mediated Bacterial Killing of Group B Streptococcus

Abstract

Dexamethasone use is sometimes associated with an increased risk of infection. Group B streptococcus (GBS) is a significant cause of infection in immunocompromised adults, pregnant woman, and neonates. Neutrophil-mediated bacterial killing is an important defense against GBS infection. We hypothesized that dexamethasone would affect neutrophil-mediated bacterial killing of GBS and studied this in vitro. Neutrophils isolated from healthy adults and neonates were either 1) incubated with dexamethasone concentrations from 0 to 100 μg/mL in the presence of GBS, complement, and antibody; or 2) incubated only with similar concentrations of dexamethasone for 1 hour, then incubated with GBS, complement, and antibody. Colony counts were performed, bacterial killing calculated, and results expressed as the log antibody-1 level at which the largest reciprocal dilution promoted ≥ 90% bacterial killing. Adult neutrophil-mediated bacterial killing was not affected by dexamethasone exposure during the bacterial killing assay but neutrophil exposure to dexamethasone before the assay resulted in improved killing (p < 0.05). Neonatal neutrophil-mediated bacterial killing was significantly decreased with dexamethasone exposure during the bacterial killing assay (p < 0.05), whereas neutrophil exposure before the assay suggested an increase in bacterial killing. All these effects were concentration dependent. Dexamethasone affects the adult and neonatal neutrophil-mediated bacterial killing of GBS in vitro. The interaction of corticosteroids, neutrophils, and bacteria appears complex and dependent on the timing of these interactions, population of neutrophils, and dexamethasone concentration. These factors may account for the variable susceptibility and response to infection associated with corticosteroids.