Studies on gallium accumulation in inflammatory lesions: I. Gallium uptake by human polymorphonuclear leukocytes.

The mechanism of ionic gallium-67 localization in inflammatory lesions was studied. Human polymorphonuclear leukocytes (PMN) had higher Ga-67 uptake than lymphocytes, whereas red blood cells had no affinity for Ga-67. Uptake by PMN showed temperature dependence, was independent of Ga-67 concentrations, and was not inhibited by metabolic inhibitors. However, its binding to PMN could be removed by trypsin but not by neuraminidase. These results are consistent with the hypothesis that the plasma membrane serves as a diffusion barrier and Ga-67 only binds to the surface of the PMN plasma membrane. When this membrane's permeability barrier was disrupted, as in heat-killed PMN, Ga-67 uptake increased markedly. Experimental abscesses were induced with E. coli or turpentine in rabbits. Twenty-four hours after i.v. injection, only 20% of Ga-67 in abscesses was in fractions containing intact PMN, cell debris or bacteria; the remainder was in a soluble, non-cellular fraction (2,500-g supernatant).