English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

Single cell phenotyping reveals heterogeneity among haematopoietic stem cells following infection.

MPS-Authors
/persons/resource/persons208298

Liepe,  J.
Research Group of Quantitative and System Biology, MPI for Biophysical Chemistry, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)

2473158.pdf
(Publisher version), 1001KB

Supplementary Material (public)

2473158_Suppl_1.pdf
(Supplementary material), 2MB

2473158_Suppl_2.pdf
(Supplementary material), 282KB

2473158_Suppl_3.pdf
(Supplementary material), 41KB

2473158_Suppl_4.pdf
(Supplementary material), 41KB

Citation

MacLean, A. L., Smith, M. A., Liepe, J., Sim, A., Khorshed, R., Rashidi, N. M., et al. (2017). Single cell phenotyping reveals heterogeneity among haematopoietic stem cells following infection. Stem Cells, 35(11), 2292-2304. doi:10.1002/stem.2692.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002D-D18D-E
Abstract
The haematopoietic stem cell (HSC) niche provides essential micro-environmental cues for the production and maintenance of HSCs within the bone marrow. During inflammation, haematopoietic dynamics are perturbed, but it is not known whether changes to the HSC-niche interaction occur as a result. We visualise HSCs directly in vivo, enabling detailed analysis of the 3D niche dynamics and migration patterns in murine bone marrow following Trichinella spiralis infection. Spatial statistical analysis of these HSC trajectories reveals two distinct modes of HSC behaviour: (i) a pattern of revisiting previously explored space, and (ii) a pattern of exploring new space. Whereas HSCs from control donors predominantly follow pattern (i), those from infected mice adopt both strategies. Using detailed computational analyses of cell migration tracks and life-history theory, we show that the increased motility of HSCs following infection can, perhaps counterintuitively, enable mice to cope better in deteriorating HSC-niche micro-environments following infection.