According to the theoretical formulation of Fenn (1921) , based in part on the previous work of Tait (1918) and Rhumbler (1914) , a decrease in free surface energy occurs when a particle is ingested by a phagocyte. Mudd and Mudd (1933) offered experimental evidence in support of this concept in their elucidation of the role played by opsonins (and nonimmune serum) in promoting phagocytosis. Bacteria in the presence of serum are more readily ingested because their surface energy is increased,

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... hence a greater decrease in energy results when they are phagocytosed. An extensive discussion of this relationship is found in the review of Mudd, McCutcheon, and Luck6 (1934). Theoretically, however, phagocytic activity should be subject to variations arising from changes in surface energy, not only of the particles being ingested, but also of the phagocytic cells themselves. Such changes have been suggested as the underlying cause of the increased phagocytosis observed in the granulocytic leucocytes of anemic human beings (Berry, Davis, and Spies, 1945; Berry, Leyendecker, and Spies, 1947) and of rats made anemic by blood loss (Berry and Haller, 1947a) . This may also explain the results of Gordon and Katsh (1949) , who found that in adrenalectomized rats the splenic macrophages take up less thorotrast (a colloidal solution of thorium dioxide) than those in normal control animals, whereas injections of adrenal cortical extract increase the macrophagic activity over that of controls. Therefore, since phagocytes are known to exhibit a variation in activity under conditions that appear to leave the particles unchanged, it is possible that changes in surface energy are involved. In order to test the validity of this hypothesis the effect of surface-active agents on the phagocytic function of neutrophilic granulocytes was investigated. The results are described in this report and are offered as additional evidence for the validity of the Fenn theory of phagocytosis. METHOD The phagocytic activity of blood neutrophiles was determined by a modification of the in vitro technique of Boerner and Mudd (1935), which has been described in detail in previous publications (Berry, Davis, and Spies, 1945; Berry, Leyendecker, and Spies, 1947) . Whole blood is diluted with an equal volume of physiological solution of sodium chloride contained in a parained test tube to which a measured volujme of standardized bacterial suspension is added.