| First Author | Valet C | Year | 2022 |
| Journal | J Clin Invest | Volume | 132 |
| Issue | 7 | PubMed ID | 35192546 |
| Mgi Jnum | J:325582 | Mgi Id | MGI:7261107 |
| Doi | 10.1172/JCI153920 | Citation | Valet C, et al. (2022) Sepsis promotes splenic production of a protective platelet pool with high CD40 ligand expression. J Clin Invest 132(7):e153920 |
| abstractText | Platelets have a wide range of functions including critical roles in hemostasis, thrombosis, and immunity. We hypothesized that during acute inflammation, such as in life-threatening sepsis, there are fundamental changes in the sites of platelet production and phenotypes of resultant platelets. Here, we showed during sepsis that the spleen was a major site of megakaryopoiesis and platelet production. Sepsis provoked an adrenergic-dependent mobilization of megakaryocyte-erythrocyte progenitors (MEPs) from the bone marrow to the spleen, where IL-3 induced their differentiation into megakaryocytes (MKs). In the spleen, immune-skewed MKs produced a CD40 ligandhi platelet population with potent immunomodulatory functions. Transfusions of post-sepsis platelets enriched from splenic production enhanced immune responses and reduced overall mortality in sepsis-challenged animals. These findings identify a spleen-derived protective platelet population that may be broadly immunomodulatory in acute inflammatory states such as sepsis. |
