The determination of the level of leukocytes in the blood stream with inflammation; a thermostable component concerned in the mechanism of leukocytosis.

W ITH AN acute inflammation the level ofwhite cells in the circulation is a!tered, but it is difficult to predict the direction of the shift. There either may be an increase or a decrease in the number of circulating leukocytes; on the other hand there may be no appreciable change. The rise is in part due to the liberation by cells, severely injured at the site of an acute inflammation, of a specific type of alpha globulins* termed as an entity, the leukocytosis-promoting factor ( 1 , 2 . 3 Subsequent work has revealed that the active principle responsible for the effect of the LPF seems to be a pe4 The rise in the number of white blood cells accompanying an inflammation cannot always be duplicated in magnitude by a single injection of the LPF. It is true that the constant production of the factor at the site of an acute inflammation may in part explain the level rising at times far above that obtained by merely injecting one dose of the LPF. On the other hand, it is conceivable that there may be other factors involved to explain the ultimate effect on the leukocyte level accompanying an acute inflammation. Earlierstudies haverevealed that subsequent tothe injectionofthewhole euglobulin of an exudate, there often develops a At the time, it was surmised that necrosin associated with the euglobulin fraction of an usually acid exudate by inducing tissue injury, in turn causes the local release of the leukocytosis-promoting factor with the eventual effect noticed.5 This proved, however, to be an incorrect interpretation, for when necrosin was eliminated from the euglobulin fraction, the noninjurious pyrexin or the pyrogenic factor of exudates still displayed the subsequent leukocytosis.6 The purpose of the present paper is twofold. In the first place, it will be shown that besides the thermolabile LPF of exudates,’ there is also present a thermostable component, especially in acid exudates, which aids in explaining the mechanism of the final leukocytosis with inflammation. In the second place, an attempt will be made to point out the various factors concerned in the determination of the white blood cell level when there is a concomitant acute inflammation. It will be shown that the final picture is a resultant of the effect of the various factors previously described,7 as well as the effect of the present component.