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The role of CSF1R-dependent macrophages in control of the intestinal stem-cell niche

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  • Anuj Sehgal

    (University of Edinburgh, Easter Bush)

  • David S. Donaldson

    (University of Edinburgh, Easter Bush)

  • Clare Pridans

    (University of Edinburgh, Easter Bush
    The Queen’s Medical Research Institute)

  • Kristin A. Sauter

    (University of Edinburgh, Easter Bush)

  • David A. Hume

    (University of Edinburgh, Easter Bush
    The Queen’s Medical Research Institute
    Translational Research Institute)

  • Neil A. Mabbott

    (University of Edinburgh, Easter Bush)

Abstract

Colony-stimulating factor 1 (CSF1) controls the growth and differentiation of macrophages.CSF1R signaling has been implicated in the maintenance of the intestinal stem cell niche and differentiation of Paneth cells, but evidence of expression of CSF1R within the crypt is equivocal. Here we show that CSF1R-dependent macrophages influence intestinal epithelial differentiation and homeostasis. In the intestinal lamina propria CSF1R mRNA expression is restricted to macrophages which are intimately associated with the crypt epithelium, and is undetectable in Paneth cells. Macrophage ablation following CSF1R blockade affects Paneth cell differentiation and leads to a reduction of Lgr5+ intestinal stem cells. The disturbances to the crypt caused by macrophage depletion adversely affect the subsequent differentiation of intestinal epithelial cell lineages. Goblet cell density is enhanced, whereas the development of M cells in Peyer’s patches is impeded. We suggest that modification of the phenotype or abundance of macrophages in the gut wall alters the development of the intestinal epithelium and the ability to sample gut antigens.

Suggested Citation

  • Anuj Sehgal & David S. Donaldson & Clare Pridans & Kristin A. Sauter & David A. Hume & Neil A. Mabbott, 2018. "The role of CSF1R-dependent macrophages in control of the intestinal stem-cell niche," Nature Communications, Nature, vol. 9(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03638-6
    DOI: 10.1038/s41467-018-03638-6
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