Neutrophils scan for activated platelets to initiate inflammation

Science  05 Dec 2014:
Vol. 346, Issue 6214, pp. 1234-1238
DOI: 10.1126/science.1256478

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Immune and inflammatory responses require leukocytes to migrate within and through the vasculature, a process that is facilitated by their capacity to switch to a polarized morphology with an asymmetric distribution of receptors. We report that neutrophil polarization within activated venules served to organize a protruding domain that engaged activated platelets present in the bloodstream. The selectin ligand PSGL-1 transduced signals emanating from these interactions, resulting in the redistribution of receptors that drive neutrophil migration. Consequently, neutrophils unable to polarize or to transduce signals through PSGL-1 displayed aberrant crawling, and blockade of this domain protected mice against thromboinflammatory injury. These results reveal that recruited neutrophils scan for activated platelets, and they suggest that the neutrophils’ bipolarity allows the integration of signals present at both the endothelium and the circulation before inflammation proceeds.

A two-cell collaboration for inflammation

Immune cells called neutrophils are first responders to infection. Neutrophils move within and through blood vessels to get to sites of infection quickly. Sreeramkumar et al. found that mouse neutrophils rely on platelets to help find such sites. Neutrophils extended protrusions into blood vessels. When these protrusions came into contact with platelets, the neutrophils migrated into the surrounding tissue to carry out their inflammatory functions. Preventing these neutrophilplatelet interactions alleviated collateral inflammatory damage to tissues in several injury models in mice.

Science, this issue p. 1234

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