Cutting edge: bacterial infection induces hematopoietic stem and progenitor cell expansion in the absence of TLR signaling.

ABSTRACT: Bone marrow (BM) hematopoietic stem and progenitor cells (HSPCs) can be activated by type I IFNs, TLR agonists, viruses, and bacteria to increase hematopoiesis. In this study, we report that endotoxin treatment in vivo induces TLR4, MyD88, and Toll/IL-1 resistance domain-containing adaptor-inducing IFN-beta (TRIF)-dependent expansion of BM HSPCs. Bacterial infection by Staphylococcus aureus or cecal ligation and puncture also induces HSPC expansion, but MyD88, TRIF, type I IFN, cytokine, PG, or oxidative stress pathways are not required for their expansion. S. aureus-induced HSPC expansion in MyD88(-/-)TRIF(-/-) mice is also normal, but is associated with BM remodeling as granulocyte stores are released peripherally. Importantly, reduction in BM cellularity alone can reproduce HSPC expansi

SUBMITTER: Scumpia PO 

PROVIDER: S-EPMC3837089 | biostudies-literature | 2010 Mar

REPOSITORIES: biostudies-literature