In silico analysis of myeloid cells across animal kingdom reveal neutrophil evolution by colony stimulating factors

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Abstract

Neutrophils constitute the largest population of phagocytic granulocytes in the blood of mammals. The development and function of neutrophils and monocytes is primarily governed by the granulocyte colony-stimulating factor receptor family (CSF3R/CSF3) and macrophage colony-stimulating factor receptor family (CSF1R/IL34/CSF1) respectively. Using various techniques this study considered how the emergence of receptor:ligand pairings shaped the distribution of blood myeloid cell populations. Comparative gene analysis supported the ancestral pairings of CSF1R/IL34 and CSF3R/CSF3, and the emergence of CSF1 later in lineages after the advent of Jawed/Jawless fish. Further analysis suggested that the emergence of CSF3 lead to reorganisation of granulocyte distribution between amphibian and early reptiles. However, the advent of endothermy likely contributed to the dominance of the neutrophil/heterophil in modern-day mammals and birds. In summary, we show that the emergence of CSF3R/CSF3 was a key factor in the subsequent evolution of the modern-day mammalian neutrophil.

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All data generated or analysed during this study are included in the manuscript and supporting files

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Damilola Pinheiro

Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom

For correspondence
d.pinheiro@imperial.ac.uk

Competing interests
The authors declare that no competing interests exist.
Marie-Anne Mawhin

Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom

Competing interests
The authors declare that no competing interests exist.
Maria Prendecki

Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0001-7048-7457
Kevin J Woollard

Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom

For correspondence
k.woollard@imperial.ac.uk

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-9839-5463

Funding

Medical Research Council (MR/M003159/1)

Kevin J Woollard

Kidney Research UK (RP_019_20160303)

Kevin J Woollard

Kidney Research UK (RP_002_20170914)

Kevin J Woollard

British Heart Foundation (PG/18/41/33813)

Kevin J Woollard

The authors declare that there was no direct funding for this work. Grants from MRC (MR/M003159/1), Kidney Research UK (RP_019_20160303, RP_002_20170914) and BHF (PG/18/41/33813) support the Woollard labKJW is now an employee for AstraZeneca (BioPharmaceuticals R&D, Cambridge, UK). All of this work was performed at Imperial College London. No funding or support was received from AstraZeneca.

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