Platelets (green) produce IL-1β (red) during a clotting reaction.

Platelets get no respect. Traditionally, these anucleate cells have been acknowledged as critical mediators of blood clotting, but they were considered metabolically challenged drones, incapable of signal-dependent gene expression. Now, Lindemann et al. (page 485) demonstrate that platelets are not only able to translate preformed mRNAs in response to environmental signals, they may also provide an important link between the coagulation and inflammatory cascades via regulated production of an inflammatory cytokine.

Using an arrayed cDNA library, the authors identified a variety of mRNAs present in resting platelets, including one encoding the interleukin-1β (IL-1β) precursor. Activation of the platelets as in clot formation triggers IL-1β production; the IL-1β then induces adhesiveness of endothelial cells for neutrophils, an inflammatory reaction. The platelet- produced IL-1β accumulates over a period of several hours, indicating that platelets can exert long-term influence over an inflammatory response. Previous work had shown that activated platelets could synthesize new proteins, but the new study is the first demonstration that the cells can inducibly produce physiologically relevant levels of cytokines.

The results suggest that platelets may be more important in mediating pathological responses than was previously recognized. Myocardial infarction, for example, begins with platelet deposition near a ruptured atherosclerotic plaque, followed by leukocyte infiltration. If the synthesis of IL-1β by the platelets is facilitating leukocyte accumulation, this signal might be a good therapeutic target. ▪