THE FATE OF EOSINOPHILS IN HORMONALLY INDUCED EOSINOPENIA AND ITS SIGNIFICANCE

Abstract

1. It is suggested that some of the circulating blood eosinophils are originally produced in the epithelial lining of the lower parts of the intestinal crypts, mainly in the small intestine but to a lesser extent in the colon. This cellular reaction may result from the penetration by the antigenic unsplit protein molecule from the lumen of the intestine into the epithelial cells, transforming these into new histological and biological units. 2. This process takes place in the normal intestinal mucosa. It is strongly intensified by the ingestion of antigenic proteins and various traumata inflicted on the intestinal canal. 3. White mice fed with de-antigenized proteins do not form a lymphocytic barrier in the lamina propria mucosae; eosinophils do not appear there until antigenic proteins are introduced into the diet. 4. Heparinization to a higher level than is required for the prevention of blood clotting, done prior to the injection of hormones causing eosinopenia, abolishes or significantly diminishes circulating eosinopenia or may actually increase the number of circulating eosinophils. Fluctuations result from two independent actions: mobilization of tissue eosinophils by heparin, and destruction of eosinophils by steroids in the circulating blood. 5. The eosinolytic action of adrenocortical steroids results from mediation in the catabolic phase of the intracellular metabolism of proteins. This action has been demonstrated in all white cells of the blood. 6. Hormonally induced eosinopenia, in men and in dogs, results from the eosinolysis which takes place in the blood. The other white blood cells are also affected by the same action. The final number of polymorphs is masked by their mobilization set up by cortical steroids through some unknown mechanism. Lymphocytes are less sensitive than eosinophils to the lytic action of cortical steroids.