Plasmacellular lymphadenopathy produced in rats by tin

Abstract

Metallic tin powder induced granulomatous inflammation at the site of inoculation and in draining lymph nodes. In addition, draining nodes were greatly enlarged by proliferation of plasma cells and Russell body cells. Granulomatous response was common to many strains of rats, but only Lewis rats developed striking plasmacellular hyperplasia, and it lasted only about 3 weeks. The spontaneous abatement of the plasma cell response was not due to corrosion of the tin in vivo because tin particles recovered from the tissues 2 weeks after inoculation were still able to induce plasma cells. Treatment of tin with heat, organic solvents, or several oxidizing and reducing reagents did not destroy its potency, but some chemicals diminished its effectiveness by inducing aggregation or stickiness. Other metals, and compounds of tin, did not produce the same reaction. Tin-treated rats had elevated serum IgG but the immunological significance of the plasma cell hyperplasia remains to be elucidated. Although plasmacellular lymphadenopathy was obtained only during a restricted period after inoculation of large doses of tin into a peculiarly susceptible animal, it does have a bearing on the putative role of tin as an essential nutrient and it will be a useful model for study of plasma cell hyperplasia.