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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Cutting edge: LPS-induced emergency myelopoiesis depends on TLR4-expressing nonhematopoietic cells.
J. Immunol. 188, 5824-5828 (2012)
Verlagsversion Volltext
DOI
PMC
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.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
Altmetric
5.788
1.339
92
99
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern
Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Colony-stimulating Factor; Mouse Bone-marrow; Progenitor Cells; G-csf; Mice; Granulocyte; Receptor; Identification; Infection; Granulopoiesis
Sprache
englisch
Veröffentlichungsjahr
2012
HGF-Berichtsjahr
2012
ISSN (print) / ISBN
0022-1767
e-ISSN
1550-6606
Zeitschrift
Journal of Immunology
Quellenangaben
Band: 188,
Heft: 12,
Seiten: 5824-5828
Verlag
American Association of Immunologists
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Virology (VIRO)
POF Topic(s)
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er)
Immune Response and Infection
PSP-Element(e)
G-551600-001
PubMed ID
22586037
WOS ID
WOS:000305077900005
Erfassungsdatum
2012-06-28