Trauma Induces Emergency Hematopoiesis through IL-1/MyD88-Dependent Production of G-CSF.

J Immunol 2019 05 15;202(10):3020-3032. Epub 2019 Apr 15.

Department of Surgery, Washington University School of Medicine in St. Louis, St. Louis, MO 63110; and

The inflammatory response to infection or injury dramatically increases the hematopoietic demand on the bone marrow to replace effector leukocytes consumed in the inflammatory response. In the setting of infection, pathogen-associated molecular patterns induce emergency hematopoiesis, activating hematopoietic stem and progenitor cells to proliferate and produce progeny for accelerated myelopoiesis. Sterile tissue injury due to trauma also increases leukocyte demand; however, the effect of sterile tissue injury on hematopoiesis is not well described. We find that tissue injury alone induces emergency hematopoiesis in mice subjected to polytrauma. This process is driven by IL-1/MyD88-dependent production of G-CSF. G-CSF induces the expansion of hematopoietic progenitors, including hematopoietic stem cells and multipotent progenitors, and increases the frequency of myeloid-skewed progenitors. To our knowledge, these data provide the first comprehensive description of injury-induced emergency hematopoiesis and identify an IL-1/MyD88/G-CSF-dependent pathway as the key regulator of emergency hematopoiesis after injury.

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http://www.jimmunol.org/lookup/doi/10.4049/jimmunol.1801456
Publisher Site
http://dx.doi.org/10.4049/jimmunol.1801456DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6504560PMC
May 2019
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