Role of macrophages in mobilization of hematopoietic progenitor cells from bone marrow after hemorrhagic shock

Meng Xiang, Youzhong Yuan, Liyan Fan, Yuehua Li, Aijun Li, Lianhua Yin, Melanie J. Scott, Guozhi Xiao, Timothy R. Billiar, Mark A. Wilson, Jie Fan*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

The release of hematopoietic progenitor cells (HPCs) from bone marrow (BM) is under tight homeostatic control. Under stress conditions, HPCs migrate from BM and egress into circulation to participate in immune response, wound repair, or tissue regeneration. Hemorrhagic shock with resuscitation (HS/R), resulting from severe trauma and major surgery, promotes HPC mobilization from BM, which, in turn, affects post-HS immune responses. In this study, we investigated the mechanism of HS/R regulation of HPC mobilization from BM. Using a mouse HS/R model, we demonstrate that the endogenous alarmin molecule high-mobility group box 1 mediates HS/R-induced granulocyte colony-stimulating factor secretion from macrophages (M in a RAGE [receptor for advanced glycation end products] signaling-dependent manner. Secreted granulocyte colony-stimulating factor, in turn, induces HPC egress from BM. We also show that activation of β-adrenergic receptors on M by catecholamine mediates the HS/R-induced release of high-mobility group box 1. These data indicate that HS/R, a global ischemia-reperfusion stimulus, regulates HPC mobilization through a series of interacting pathways that include neuroendocrine and innate immune systems, in which M play a central role.

Original languageEnglish
Pages (from-to)518-523
Number of pages6
JournalShock
Volume37
Issue number5
DOIs
StatePublished - May 2012
Externally publishedYes

Keywords

  • "-adrenergic receptor
  • G-CSF
  • HMGB1
  • Innate immune
  • RAGE

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