Accumulation of gallium-67 inflammatory lesions has been well documented. However, little is known about the mechanism by which gallium is localized in inflammatory lesions. We have studied in-vitro uptake of gallium by human polymorphonuclear leukocytes and a variety of micro-organisms, the main components of inflammatory lesions. We also developed an animal model which will allow us to sample the inflammatory exudate repeatedly for analysis. We propose to extend our observation and explore further the mechanisms of gallium accumulation in inflammatory lesions. Our specific aims are: 1) study and identify the intracellular protein(s) which binds gallium disruption of human polymorphonuclear leukocytes membrane permeability barrier, 2) study the role of lactoferrin and transferrin in the binding of gallium in human plasma, and 3) using the newly developed animal model, to study 1) the role of polymorphonuclear leukocytes and bacteria in the accumulation of gallium in inflammatory lsions, b) kinetic of gallium accumulation and c) the protein(s) which binds gallium in the 2,500 g supernate of the inflammatory exudate.