Unknown

Dataset Information

0

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 expansion. These data show in vivo HSPC responses to bacterial infection are complex and not absolutely dependent upon key inflammatory signaling pathways.

SUBMITTER: Scumpia PO 

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

REPOSITORIES: biostudies-literature

Json Xml
altmetric image

Publications

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

Scumpia Philip O PO   Kelly-Scumpia Kindra M KM   Delano Matthew J MJ   Weinstein Jason S JS   Cuenca Alex G AG   Al-Quran Samer S   Bovio Ian I   Akira Shizuo S   Kumagai Yutaro Y   Moldawer Lyle L LL  

Journal of immunology (Baltimore, Md. : 1950) 20100203 5

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  ...[more]

Similar Datasets

Unknown Cutting Edge: Hematopoietic Stem Cell Expansion and Common Lymphoid Progenitor Depletion Require Hematopoietic-Derived, Cell-Autonomous TLR4 in a Model of Chronic Endotoxin.
| S-EPMC4561199 | biostudies-literature
Unknown Chemical Cocktail Induces Hematopoietic Reprogramming and Expands Hematopoietic Stem/Progenitor Cells.
| S-EPMC6947705 | biostudies-literature
Unknown Cutting Edge: Plasmodium falciparum Induces Trained Innate Immunity.
| S-EPMC5927587 | biostudies-literature
Unknown Cutting edge: TLR signaling licenses IRAK1 for rapid activation of the NLRP3 inflammasome.
| S-EPMC3924784 | biostudies-literature
Unknown MyD88-dependent TLR signaling oppositely regulates hematopoietic progenitor and stem cell formation in the embryo.
| S-EPMC8935211 | biostudies-literature
Unknown Cutting edge: accelerated autoimmune diabetes in the absence of LAG-3.
| S-EPMC3178660 | biostudies-literature
Unknown Spheroid Coculture of Hematopoietic Stem/Progenitor Cells and Monolayer Expanded Mesenchymal Stem/Stromal Cells in Polydimethylsiloxane Microwells Modestly Improves In Vitro Hematopoietic Stem/Progenitor Cell Expansion.
| S-EPMC5397247 | biostudies-literature
Unknown Endothelial progenitor cell infusion induces hematopoietic stem cell reconstitution in vivo.
| S-EPMC2651019 | biostudies-literature
Unknown Cutting edge: Hematopoietic-derived APCs select regulatory T cells in thymus.
| S-EPMC3325783 | biostudies-literature
Unknown Dnmt3a regulates myeloproliferation and liver-specific expansion of hematopoietic stem and progenitor cells.
| S-EPMC4856586 | biostudies-literature