Header

UZH-Logo

Maintenance Infos

Sensing and translation of pathogen signals into demand-adapted myelopoiesis


Boettcher, S; Manz, M G (2016). Sensing and translation of pathogen signals into demand-adapted myelopoiesis. Current Opinion in Hematology, 23(1):5-10.

Abstract

PURPOSE OF REVIEW: During severe systemic infection, steady-state hematopoiesis is switched to demand-adapted myelopoiesis, leading to increased myeloid progenitor proliferation and, depending on the context and type of pathogen, enhanced granulocytic or monocytic differentiation, respectively. We will review the recent advances in understanding direct and indirect mechanisms by which different pathogen signals are detected and subsequently translated into demand-adapted myelopoiesis.
RECENT FINDINGS: Enhanced myeloid progenitor proliferation and neutrophil differentiation following infection with prototypic Gram-negative bacterium Escherichia coli is mediated by granulocyte colony-stimulating factor, and reactive oxygen species released from endothelial cells and mature myeloid cells, respectively. Furthermore, hematopoietic stem and progenitor cells directly sense pathogen signals via Toll-like receptors and contribute to emergency granulopoiesis via release and subsequent autocrine and paracrine action of myelopoietic cytokines including IL-6. Moreover, emergency monocytopoiesis upon viral infection depends on T cell-derived IFNγ and release of IL-6 from bone marrow stromal cells.
SUMMARY: A complex picture is evolving in which various hematopoietic and nonhematopoietic cell types interact with the hematopoietic system in an intricate manner to shape an appropriate hematopoietic response to specific infectious stimuli.

Abstract

PURPOSE OF REVIEW: During severe systemic infection, steady-state hematopoiesis is switched to demand-adapted myelopoiesis, leading to increased myeloid progenitor proliferation and, depending on the context and type of pathogen, enhanced granulocytic or monocytic differentiation, respectively. We will review the recent advances in understanding direct and indirect mechanisms by which different pathogen signals are detected and subsequently translated into demand-adapted myelopoiesis.
RECENT FINDINGS: Enhanced myeloid progenitor proliferation and neutrophil differentiation following infection with prototypic Gram-negative bacterium Escherichia coli is mediated by granulocyte colony-stimulating factor, and reactive oxygen species released from endothelial cells and mature myeloid cells, respectively. Furthermore, hematopoietic stem and progenitor cells directly sense pathogen signals via Toll-like receptors and contribute to emergency granulopoiesis via release and subsequent autocrine and paracrine action of myelopoietic cytokines including IL-6. Moreover, emergency monocytopoiesis upon viral infection depends on T cell-derived IFNγ and release of IL-6 from bone marrow stromal cells.
SUMMARY: A complex picture is evolving in which various hematopoietic and nonhematopoietic cell types interact with the hematopoietic system in an intricate manner to shape an appropriate hematopoietic response to specific infectious stimuli.

Statistics

Citations

Dimensions.ai Metrics
13 citations in Web of Science®
12 citations in Scopus®
11 citations in Microsoft Academic
Google Scholar™

Altmetrics

Downloads

13 downloads since deposited on 30 Jan 2017
13 downloads since 12 months
Detailed statistics

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Hematology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:23 January 2016
Deposited On:30 Jan 2017 13:35
Last Modified:02 Feb 2018 11:49
Publisher:Lippincott Williams & Wilkins
ISSN:1065-6251
OA Status:Green
Publisher DOI:https://doi.org/10.1097/MOH.0000000000000201
PubMed ID:26554891

Download

Download PDF  'Sensing and translation of pathogen signals into demand-adapted myelopoiesis'.
Preview
Content: Updated Version
Filetype: PDF
Size: 732kB
View at publisher