Adam Lab

Our Mission

Our Mission is to find novel therapeutics to treat tissue damage and organ dysfunction caused by disproportionate inflammatory responses. We aim to achieve that by identifying the most critical mechanisms of the pathophysiology that lead to chronic and excessive inflammation. 

Our research - When inflammation goes awry

A cytokine-driven acute increase in vascular permeability is an essential feature of the inflammatory response leading to tissue repair and pathogen clearance. However, sustained vascular leakage due to prolonged or exacerbated inflammation leads to organ damage, lasting sequelae and increased mortality. The mechanism mediating the acute (minutes to hours) responses to proinflammatory cytokine signaling are well-described: phosphorylation of tyrosines in adherens junction proteins and an increase in actin-myosin contractility are two main mechanisms leading to a quick loss of endothelial intercellular adhesion and thus an increase in vascular permeability. Despite its importance in severe and chronic inflammation, little is known about the changes in the endothelium causing a sustained (lasting hours to days) vascular barrier breakdown. Understanding these long-term mechanisms may prove crucial to allow us to directly target vascular leakage and minimize tissue damage, thus reducing the rates of mortality and chronic sequelae of excessive edema.

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We are grateful for our current and past funding from: