Differential increase in 12-HETE release and CD29/CD49f expression of platelets from normal donors and from patients with atopic dermatitis by Staphylococcus aureus.

The generation of the arachidonic acid-derived inflammatory mediator 12-hydroeicosatetraenoic acid (HETE) and the expression of CD29 as well as CD49f from unstimulated and stimulated platelets has been studied in patients with atopic dermatitis (AD) as well as in healthy volunteers. Heat-killed clinical isolates of Staphylococcus aureus served as stimuli. Unstimulated platelets from patients with AD produced higher amounts of 12-HETE compared to platelets from normal donors. The absolute 12-HETE release from platelets of patients with AD was significantly higher compared to the control group after stimulation with heat-killed S. aureus, whereas the relative increase remained. The expression of CD29 and CD49f on unstimulated platelets of patients with AD was markedly enhanced compared to platelets from normal donors. Stimulation with S. aureus led to similar results as to the CD29 expression on normal and atopic platelets or to a markedly higher expression of CD49f on platelets from normal donors. As compared to platelets from normal donors the CD49f expression on atopic platelets was slightly enhanced by S. aureus. Our data emphasize that platelets may play an important role in the pathogenesis of AD by an increased preactivation and by an enhanced responsiveness to S. aureus which colonizes permanently the skin of patients with AD.