DEXAMETHASONE AFFECTS THE NEUTROPHIL-MEDIATED BACTERIAL KILLING OF GROUP-B STREPTOCOCCUS

Dexamethasone use is sometimes associated with an increased risk of in fection. Group B streptococcus (GBS) is a significant cause of infecti on in immunocompromised adults, pregnant woman, and neonates. Neutroph il-mediated bacterial killing is an important defense against GBS infe ction. We hypothesized that dexamethasone would affect neutrophil-medi ated bacterial killing of GBS and studied this in vitro. Neutrophils i solated from healthy adults and neonates were either 1) incubated with dexamethasone concentrations from 0 to 100 mu g/mL in the presence of GBS, complement, and antibody; or 2) incubated only with similar conc entrations of dexamethasone for 1 hour, then incubated with GBS, compl ement, and antibody. Colony counts were performed, bacterial killing c alculated, and results expressed as the log antibody-l level at which the largest reciprocal dilution promoted greater than or equal to 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 k illing was significantly decreased with dexamethasone exposure during the bacterial killing assay (p < 0.05), whereas neutrophil exposure be fore the assay suggested an increase in bacterial killing. All these e ffects were concentration dependent. Dexamethasone affects the adult a nd neonatal neutrophil-mediated bacterial killing of GBS in vitro. The interaction of corticosteroids, neutrophils, and bacteria appears com plex and dependent on the timing of these interactions, population of neutrophils, and dexamethasone concentration. These factors may accoun t for the variable susceptibility and response to infection associated with corticosteroids.