The Biochemical Basis of Phagocytosis

Abstract

For many decades the phenomenon of phagocytosis has been of prime interest to medical scientists as an important factor in the defense of the host in infectious disease (1, 2). As a manifestation of cellular activity, it has also held the interest of biologists in general. However, the biochemical mechanisms that underlie the ingestion of relatively large particles by phagocytes have not been systematically studied. Occasional reports have appeared in the literature which indicated a transient increase in oxygen uptake by leukocytes during phagocytosis (3-5). During studies of the host-parasite relationship in our laboratory (6-8), a dramatic increase in the oxygen uptake rates of polymorphonuclear leukocytes or monocytes was observed while tubercle bacilli were being ingested. Such observations might be interpreted as offering evidence contrary to widely held opinions that phagocytosis is a process which does not require a specific expenditure of energy on the part of the phagocytizing cell (9, 10). The present paper contains results of a study of some changes in the metabolic patterns of leucocytes which occur during the phagocyticl event. In particular the relationship between glucose metabolism and phagocytosis, and the influence of various inhibitors on both processes, have been examined. Preliminary reports have appeared previously (11-13).