Michael Seeds, Ph.D.


Projects in Dr. Seeds’ laboratory seek to understand how otherwise normal innate immune functions of granulocytes contribute to tissue injury and inflammation in the context of lung diseases, such as ARDS and asthma. The current focus is the regulation and activation of secretory phospholipase A2 enzymes that hydrolyze phospholipid membranes in and on target cells. Relevant membrane systems include: 1) hydrolysis of surfactant phospholipids during lung injury, 2) hydrolysis of bacterial membranes during antimicrobial host defense, 3) hydrolysis of eukaryotic cell membranes to release eicosanoid inflammatory  mediators, and 4) hydrolysis of eukaryotic cell membranes to stimulate or resolve apoptosis. My research approaches are to delineate inflammatory biochemistry from lung tissues ex vivo, and model putative mechanisms regulating sPLA2 using cell line models and recombinant proteins, in vitro. These laboratory studies utilize a variety of techniques, including molecular biology, microscopy, biochemistry, and cell physiology to understand the function and regulation of these enzymes. Collaborations include investigations of surfactant injury during asthma, granulocyte apoptosis, innate immunity, and genetic variations in sPLA2 genes which impact on pulmonary diseases. The goal of this work is to identify those granulocyte/innate immune functions that can be therapeutically abrogated during inflammation from those that should not.

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