Monocytes and macrophages play important roles in host defense against staphylococci and other pyogenic bacteria [10] , but excessive systemic or local production of inflammatory mediators by macrophages could be deleterious in patients with severe staphylococcal infections. We previously reported that RAW264.7 murine macrophages exposed to any of a series of six pediatric clinical isolates of S. aureus (two CA-MRSA, two HA-MRSA, and two methicillin-susceptible strains) in the presence of daptomycin (vs. vancomycin) secreted less TNF and accumulated less inducible nitric oxide synthase (iNOS) protein [11] . Vancomycin is a cell-wall active antibiotic that triggers bacterial lysis; it is the antibiotic most commonly used to treat severe MRSA infections in children [12] . Daptomycin is a novel antibiotic that is rapidly bactericidal against staphylococci but does not appear to cause rapid bacterial lysis; the mechanism of its action is not certain but it is reported to trigger depolarization of the bacterial membranes and inhibition of both DNA and RNA synthesis [13, 14] . The rapid lysis of staphylococci, streptococci and other pyogenic bacteria exposed to cell-wall active antibiotics such as beta-lactams and vancomycin results in exaggerated release of bacterial products and an augmented and potentially harmful host inflammatory response [15, 16] . Therefore, optimal treatment of sepsis and other severe bacterial infections might include the use of antibiotics and/or other medications that blunt the host inflammatory response and dampen the cytokine cascade [16] .