Kinin Metabolism in Normal and Malignant Leucocytes

Abstract

Figure 1 represents a typical inflammatory response in terms of the rate of migration of cellular elements of inflammation to an inflammatory site. The inflammation in this illustration was caused by the presence of glycogen in the peritoneal cavity of the rabbit. Glycogen infusion is an artificial mechanism which has been used in many laboratories to produce inflammation (1). It may be seen (note the log scale of the ordinate) that the polymorphonuclear leucocytes ar’2 the first type of leucocytes to migrate to the area of inflammation. Several hours later monocytes and lymphocytes begin to appear. These cells represent possible extra-plasma sources of chemical mediators which could influence the inflammatory response. We have looked into this possibility by investigating the various leucocytes as far as their kinin-forming and kinin-destroying eazymes and at the kinin that these enzymes could possibly make. Figure 2 demonstrates that kinin-forming enzymes in polymorphonuclear leucocytes when acting on purified kininogen produces two types of kinins(2). Avariety of studies have shown that the first kinin eluted is no doubt bradykinin while the second peak differs in a variety of respects from all know mammalian kinins.