PUBLICATION

Systemic inoculation of Escherichia coli causes emergency myelopoiesis in zebrafish larval caudal hematopoietic tissue

Authors
Hou, Y., Sheng, Z., Mao, X., Li, C., Chen, J., Zhang, J., Huang, H., Ruan, H., Luo, L., Li, L.
ID
ZDB-PUB-161113-17
Date
2016
Source
Scientific Reports   6: 36853 (Journal)
Registered Authors
Huang, Honghui, Li, Li, Luo, Lingfei, Ruan, Hua, Zhang, Jingjing
Keywords
Inflammatory diseases, Myelopoiesis
MeSH Terms
  • Animals
  • Apoptosis
  • Cell Proliferation
  • Escherichia coli/immunology*
  • Escherichia coli Infections/immunology
  • Escherichia coli Infections/microbiology
  • Escherichia coli Infections/pathology*
  • Hematopoietic Stem Cells/immunology
  • Hematopoietic Stem Cells/microbiology
  • Larva/microbiology
  • Macrophages/immunology
  • Macrophages/microbiology
  • Myelopoiesis*
  • Neutrophils/immunology
  • Neutrophils/microbiology
  • Phagocytosis
  • Zebrafish
PubMed
27833150 Full text @ Sci. Rep.
Abstract
Emergency granulopoiesis occurs in response to severe microbial infection. However, whether and how other blood components, particularly monocytes/macrophages and their progenitors, including hematopoietic stem/progenitor cells (HSPCs), participate in the process and the underlying molecular mechanisms remain unknown. In this study, we challenged zebrafish larvae via direct injection of Escherichia coli into the bloodstream, which resulted in systemic inoculation with this microbe. The reaction of hematopoietic cells, including HSPCs, in the caudal hematopoietic tissue was carefully analysed. Both macrophages and neutrophils clearly expanded following the challenge. Thus, emergency myelopoiesis, including monopoiesis and granulopoiesis, occurred following systemic bacterial infection. The HSPC reaction was dependent on the bacterial burden, manifesting as a slight increase under low burden, but an obvious reduction following the administration of an excessive volume of bacteria. Pu.1 was important for the effective elimination of the microbes to prevent excessive HSPC apoptosis in response to stress. Moreover, Pu.1 played different roles in steady and emergency monopoiesis. Although Pu.1 was essential for normal macrophage development, it played suppressive roles in emergency monopoiesis. Overall, our study established a systemic bacterial infection model that led to emergency myelopoiesis, thereby improving our understanding of the function of Pu.1 in this scenario.
Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes