First paragraph (this article has no abstract)

In a recent issue of Critical Care, Wong and colleagues [1] demonstrated that the serum concentration of IL-27 in critically ill children was a predictor of infection. Our study aims at determining whether platelet activation contributes to the elevated plasma IL-27 concentration. Here we demonstrate that activation of platelets with thrombin receptor activating peptide (TRAP) significantly increased IL-27 levels in supernatants (Figure 1a). Moreover, B cells incubated in vitro with supernatants from activated platelets upregulated membrane expression of CD86, which was restored to baseline when B cells were pre-incubated with a gp130 blocking antibody (Figure 1b). Our data strongly suggest that platelet activation contributes, along with classical sources [2], to elevated plasma levels of IL-27. Recent advances place platelets as an important link between innate and adaptive immunity [3]. Indeed, platelets modulate their inflammatory response after sensing the presence of an infectious agent [4]. Therefore, platelet activation could contribute to increased plasma concentrations of IL-27 along with cytokines such as soluble CD40L [5], and thus may contribute towards immune dysregulation in patients with sepsis.