MECHANISM OF THE AUGMENTING ACTION OF MINERAL OIL ON ANTIBODY PRODUCTION

Abstract

A comparative study was made in rabbits of antibody production and tissue changes following the injection into the foot pads, of saline in Falba and mineral oil emulsion, of killed cells of Shigella paradysenteriae Flexner in saline, and of killed cells of Shigella paradysenteriae in saline in Falba-mineral oil emulsion. It was found that antibody production was greatly prolonged by the emulsification in oil. While with antigen in saline the serum titers began to fall 9 days after injection and disappeared somewhere between the 3rd and 6th months, with antigen in paraffin oil they began to drop only after 14 days, and were still high after 10 months, when the experiment was ended. The toxic effects of the antigen were greatly reduced by the emulsification in oil. A subcutaneous dose of 1.5 mg. of antigen in saline caused mesenchymal reactions in lung, liver, and spleen as well as toxic degeneration and sometimes necrosis of the liver whereas eight times as much of the antigen in oil produced no systemic lesions. Oil drops remained detectable in the foot pad until the end of the experiment. Bacteria remained visible in the oil for 1 week or more, but with saline they disappeared within 1 day. The latter observation shows that retention of antigen at the site of injection is at least one of the mechanisms of prolongation of antibody formation by paraffin oil. The tissue reaction in the foot pad to antigen in oil was largely one of suppuration with the production of persisting mononuclear granulomata whereas after antigen in saline it was chiefly one of catarrhal inflammation, subsiding within a month. The changes in the regional lymph nodes were essentially those of lymphatic hyperplasia with the production of numerous lymphocytes and large active secondary nodules, the macrophages remaining subsidiary. The lymphocytic reaction in the lymph nodes closely paralleled the antibody response but the monocytic reaction at the site of injection was not correlated with this response; in fact, in the antigen in oil experiments the monocytic reaction reached its height after the peak of antibody production. The tissue changes observed in the various experiments were consistent with the finding previously reported from this laboratory, that the lymphocyte is concerned in antibody formation.