Distinct bone marrow-derived and tissue-resident macrophage lineages proliferate at key stages during inflammation

Luke C. Davies, Marcela Rosas, Stephen J. Jenkins, Chia-Te Liao, Martin J. Scurr, Frank Brombacher, Donald J. Fraser, Judith E. Allen, Simon A. Jones and Philip R. Taylor ()
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Luke C. Davies: Institute of Infection and Immunity, Cardiff University School of Medicine
Marcela Rosas: Institute of Infection and Immunity, Cardiff University School of Medicine
Stephen J. Jenkins: Centre for Immunity, Infection and Evolution, and the Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh
Chia-Te Liao: Institute of Infection and Immunity, Cardiff University School of Medicine
Martin J. Scurr: Institute of Infection and Immunity, Cardiff University School of Medicine
Frank Brombacher: International Center for Genetic Engineering and Biotechnology
Donald J. Fraser: Institute of Molecular and Experimental Medicine, Cardiff University School of Medicine
Judith E. Allen: Centre for Immunity, Infection and Evolution, and the Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh
Simon A. Jones: Institute of Infection and Immunity, Cardiff University School of Medicine
Philip R. Taylor: Institute of Infection and Immunity, Cardiff University School of Medicine

Nature Communications, 2013, vol. 4, issue 1, 1-10

Abstract: Abstract The general paradigm is that monocytes are recruited to sites of inflammation and terminally differentiate into macrophages. There has been no demonstration of proliferation of peripherally-derived inflammatory macrophages under physiological conditions. Here we show that proliferation of both bone marrow-derived inflammatory and tissue-resident macrophage lineage branches is a key feature of the inflammatory process with major implications for the mechanisms underlying recovery from inflammation. Both macrophage lineage branches are dependent on M-CSF during inflammation, and thus the potential for therapeutic interventions is marked. Furthermore, these observations are independent of Th2 immunity. These studies indicate that the proliferation of distinct macrophage populations provides a general mechanism for macrophage expansion at key stages during inflammation, and separate control mechanisms are implicated.

Date: 2013
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DOI: 10.1038/ncomms2877

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