Targeting tissue macrophage generation as a mechanism to modulate the resolution of inflammation.

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Tissue resident macrophages are white blood cells that are scattered throughout and live in the tissues of our body. They are at the frontline of host defense against infection in the tissue and play important roles in maintaining the normal function of the tissue itself. After an infection, macrophages are also recruited to the tissue from the blood, arriving as blood monocytes that originate from the bone marrow and turn into macrophages upon arrival. Our recent studies highlight the quite distinct origins of tissue resident and monocyte-derived macrophages. They show differences in gene expression that probably reflect not just their distinct functional programming, but also the mechanism by which tissue macrophages are programmed to survive for long periods in the tissue, and to self-renew. By manipulating specific subsets of macrophages we aim to bias responses to infection and wound repair to promote beneficial outcomes. Our proposed studies would be first proof-of-principle experiments that would examine a new avenue of research directed at the control of infection and tissue damage.