Pam J. Fraker

Our lab is interested in the interplay between nutritional status, immune defense and the neuroendocrine system. Single element deficiencies in zinc or multi-component deficiencies in protein-calories cause a rapid decline in antibody and cell mediated responses. We have shown that such deficiencies activate the neuroendocrine stress axis causing chronic production of glucocorticoids which rapidly reduce lymphopoiesis by accelerating apoptosis among pre T and pre B cells. The resulting decline in the numbers of peripheral lymphocytes impairs host defense. These changes impact malnourished children as well as those with chronic diseases where suboptimal nutriture compromises immune defense. We recently discovered a compensatory mechanism whereby the elevated glucocorticoids promote myelopoiesis. Thus, the phagocytic cells that are the first line of defense remain plentiful with retention of key functions thereby providing interim protection. Currently we are examining the dysregulation of the immune system created by obesity using the morbidly obese undergoing gastric bypass surgery and the overfed mouse as models for study. Our goal is to better understand the neuroendocrine-metabolic changes in obesity that lead to higher rates of infection, increased pneumonia, and poor wound healing.