Research Interests:
Trauma is the number one cause of death in children and the third-leading overall killer of adults in the United States. The chances of mortality after trauma are complicated by the patient’s own response to injury, which is demonstrated by exaggerated inflammatory response resulting in organ dysfunction and death. The inflammatory response after injury is modulated by several components, including the injury itself, the environment and the sex, age and genetic make-up of the patient. The main objective of our laboratory is to understand the inflammatory response after injury at the genetic and molecular levels. We are currently mapping genes that modulate the inflammatory process by using different mouse genetic resources. These genes can be used as genetic markers for identifying human patients that display a predisposition to inflammatory diseases. In addition, the molecular pathways in which these genes are involved can be investigated in isolated cell populations, such as macrophages.
Another important component of the response to injury is the expression of genes encoding heat shock or stress proteins. The presence of these proteins confers protection to cells from subsequent stresses, a phenomenon called stress tolerance. Heat shock proteins have recently been found to regulate vesicle traffic in order to remodel the cell surface. Moreover, heat shock proteins released into the extracellular milieu following necrosis act as immunomodulators by interacting with lipid membrane components, particularly lipid rafts. The mechanism involved in this process is currently under investigation, and the information generated from these studies may be of help in the care of critically ill patients.
Track(s):
Microbiology/Immunology
MCB
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