LIIIIARY ”lemon Cute University J PLACE IN RETURN BOX to remove We checkout from your record. TO AVOID FINES return on or before one due. DATE DUE DATE DUE DATE DUE LL fiflL ] MSU Is An Affirmative Action/Equal Opportunity Institution chided-damn! GR 0“. P!!! 'M 5.. STATUS OF MURINE RESIDENT PERITONEAL MACROPHAGE ANTIGEN PRESENTATION AND MICROBICIDAL CAPACITY AFTER DIETARY ZINC DEPRIVATION OR CHRONIC TREATMENT WITH PHYSIOLOGICAL LEVELS OF GLUCOCORTICOIDS IN VIVO AND IN VITRO BY Gerald Lee Morford A DISSERTATION Submitted to . Michigan State Univer51ty. in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY Department of Biochemistry 1991 STATUS PRESENT DEERE? ABSTRACT STATUS OF MURINE RESIDENT PERITONEAL MACROPHAGE ANTIGEN PRESENTATION AND MICROBICIDAL CAPACITY AFTER DIETARY ZINC DEPRIVATION OR CHRONIC TREATMENT WITH PHYSIOLOGICAL LEVELS OF GLUCOCORTICOIDS In VIVO AND IN VIIRO by Gerald Lee Morford Zinc deficiency impairs the host defense capabilities of humans and mice. Dietary zinc deprivation in mice decreases cell and antibody mediated responses, elevates plasma glucocorticoid levels and reduces numbers of immune cells. Two of the key host defense capacities of the resident macrophage were examined: the capacity to initiate humoral immune responses and microbicidal capacity. Care was taken to minimize the exposure of :macrophages to zinc in ‘vitro. Because glucocorticoids are known immunosuppressants the effects of chronic exposure to glucocorticoids at levels observed during zinc deficiency on the same macrophage capacities were also determined. Resident peritoneal macrophages from zinc deficient.mice were able to present antigen to a Th2 clone, produce membrane and soluble IL-1 activity and express Ia as well as control macrophages. Thus zinc deficiency did not appear to alter the capacity of macrophages to initiate humoral immune responses. In contrast, zinc deficiency limited the ability of