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Cutting edge: LPS-induced emergency myelopoiesis depends on TLR4-expressing nonhematopoietic cells.
J. Immunol. 188, 5824-5828 (2012)
Systemic bacterial infection is rapidly recognized as an emergency state leading to neutrophil release into the circulation and increased myeloid cell production within the bone marrow. However, the mechanisms of sensing infection and subsequent translation into emergency myelopoiesis have not been defined. In this study, we demonstrate in vivo in mice that, surprisingly, selective TLR4 expression within the hematopoietic compartment fails to induce LPS-driven emergency myelopoiesis. In contrast, TLR4-expressing nonhematopoietic cells are indispensable for LPS-induced, G-CSF-mediated myelopoietic responses. Furthermore, LPS-induced emergency myelopoiesis is independent of intact IL-1RI signaling and, thus, does not require inflammasome activation. Collectively, our findings reveal a key and nonredundant role for nonhematopoietic compartment pathogen sensing that is subsequently translated into cytokine release for enhanced, demand-adapted myeloid cell production.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Colony-stimulating Factor; Mouse Bone-marrow; Progenitor Cells; G-csf; Mice; Granulocyte; Receptor; Identification; Infection; Granulopoiesis
ISSN (print) / ISBN
0022-1767
e-ISSN
1550-6606
Journal
Journal of Immunology
Quellenangaben
Volume: 188,
Issue: 12,
Pages: 5824-5828
Publisher
American Association of Immunologists
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Virology (VIRO)