
<ArticleTitle>Stimulation of human neutrophils and monocytes by staphylococcal phenol-soluble modulin.</ArticleTitle>
<AbstractText>Modulins represent microbial products that stimulate cytokine production in host cells. The modulins responsible for gram-positive sepsis remain poorly understood. Staphylococci release a factor (or factors) that activates <prot>nuclear factor-kappa B</prot> and stimulates cytokine production in cells of macrophage lineage. This factor, termed <prot>phenol-soluble modulin</prot> (<prot>PSM</prot>), has been recently isolated from culture supernatant of Staphylococcus epidermidis. We examined the effects of <prot>PSM</prot> on proinflammatory properties of human neutrophils and monocytes in vitro. <prot>PSM</prot> activated the respiratory (oxidative) burst in neutrophils and primed neutrophils for enhanced respiratory burst activity in response to formyl-methionyl-leucyl-phenylalanine. <prot>PSM</prot> also stimulated neutrophil degranulation as reflected by increased surface expression of <prot>CD11b</prot> and <prot>CD18</prot>, which was accompanied by rapid shedding of <prot>L-selectin</prot>. Spontaneous apoptosis of both neutrophils and monocytes was inhibited by <prot>PSM</prot>. Furthermore, <prot>PSM</prot> also functioned as a chemoattractant factor for both neutrophils and monocytes. Thus, the proinflammatory properties of <prot>PSM</prot> resemble those of both lipopolysaccharide and bacterial chemotactic peptides. These findings suggest that <prot>PSM</prot> may play a role in the pathogenesis and systemic manifestations of sepsis caused by staphylococci.</AbstractText>
