Inflammation and Related Phenomena 121 



has also been shown to be associated with the aquisition by the 

 endothelium of phagocytic properties, so that colloidal particles 

 are ingested into the endothelial cytoplasm (McCluskey and Bena- 

 cerraf, 1959) . The development of stickiness and the associated 

 phenomena of leucocyte adhesion and endothelial phagocytosis is 

 probably due to changes at the surface of the endothelial cell. The 

 essential feature of these changes may be loss of normal electrical 

 negativity. Alteration in electrical charge presumably would be 

 associated with modification of the radicles, e.g. COOH groups 

 presenting at the cell surface, and such chemical alterations could 

 well be more important than loss of electrical negativity alone. In 

 any event the effect of these developments could be to inactivate 

 those forces which normally prevent adhesion of leucocytes (which 

 also carry a negative surface charge) and endothelium. The 

 mechanism of adhesion may consist of aquisition of a coating of 

 negatively charged protein by both cell surfaces, the two layers of 

 protein then uniting with the aid of calcium ions. 



The adhesion of numbers of potentially highly mobile poly- 

 morph leucocytes to endothelium together with further changes in 

 the vessel wall allowing white cells to pass between the endothelium 

 could account for much of the leucocyte emigration seen in acute 

 inflammation. This argument is the basis of the first view of the 

 mechanism of such migration. This theory suggests that the action 

 of capillary permeability factors such as histamine, peptides and 

 globulins is adequate to account not only for the passage of plasma 

 into the tissues but also of leucocytes. There are three arguments in 

 favour of this hypothesis. First, capillary permeability factors cause 

 "stickiness' of vascular endothelium; second, injection of these sub- 

 stances in high concentration leads to leucocyte emigration from 

 vessels; third, these permeability-increasing compounds do not ap- 

 pear to be chemotactic to leucocytes in vitro (Harris, 1954) . 



There are, however, powerful reasons for rejecting this theory 

 as the sole cause of leucocyte emigration. Thus varieties of inflam- 

 mation associated with comparable degrees of plasma exudation 

 vary greatly in the extent of leucocytic infiltration of the tissues. In 

 particular, certain bacterial infections, e.g. due to staphylococci lead 

 to very intense accumulation of white cells outside the vessels. 



