At steady state, resident macrophages maintain disparate aspects of tissue homeostasis relevant to tissue-specific function. For example, without resident alveolar macrophages, surfactant turnover and lung immunity are both compromised with life-threatening consequences. In the setting of injury, both sterile and infectious, multiple myeloid populations are recruited to peripheral tissues, and this heterogeneity has recently come under sharper focus with the granular analysis afforded by single cell sequencing both in mouse and human.
The goal of our laboratory is to define the functional properties of these subgroups of macrophages, and the central hypothesis is that direct contact between macrophages and tissue-specific stakeholders–fibroblasts in the remodelling lung and lung vasculature in sepsis and vascular leak among myriad examples–drives disease outcomes.
Currently, our work is supported by an investigator-initiated grant from the Department of Defense, “Targeting ATP Receptor P2RX4 for Pulmonary Fibrosis”.