122 The Chemistry of the Injured Cell 



Again, it is possible to obtain sterile tissue extracts, e.g. from 

 the uterus of oestrogen-treated mice or from five hour old burns in 

 rats, with a peculiarly powerful ability to induce leucocyte emigra- 

 tion, although the effect of such extracts on capillary permeability 

 to protein is no greater than that of other tissue extracts with little 

 action on leucocytes (Spector and Storey, 1958; Hurley and 

 Spector, 1961) . 



Finally, in non-bacterial inflammation, the time course of in- 

 creased capillary permeability to protein on the one hand and leuco- 

 cyte emigration on the other, may be quite different. In thermal and 

 chemical injury in rats the migration of polymorphs from vessels 

 does not reach its peak until the passage of plasma into the tissues is 

 declining. 



In the case of the disproportionate tissue leucocytosis of certain 

 bacterial infections, the leucocyte emigration may be attributed to 

 chemotaxis. This implies that the living or dead organisms exert a 

 positive directional "pull" on the white cells. The major evidence 

 in support of this view is the powerful chemotactic effect of pus-pro- 

 ducing organisms on leucocytes in carefully controlled systems in 

 vitro (Harris, 1954) . It may well be, however, that chemotactic 

 influences in the tissues are unable to draw leucocytes out of vessels 

 unless the vessel wall itself suffers some alteration such as occurs in 

 increased capillary permeability. Thus capillary permeability fac- 

 tors and chemotactic stimuli might work together. It is the polysac- 

 charide fraction of bacteria which is most likely to be the active 

 principle of their chemotactic action on leucocytes. Polysaccharides 

 which are chemotactic to white cells in vitro have been isolated 

 from many strains of microorganisms and also from a variety of 

 animal and plant tissues (Meier and Schar, 1957) . 



The discrepancies between increased capillary permeability and 

 leucocyte emigration in non-bacterial inflammation cannot be re- 

 solved so easily. The extent of the discrepancy is revealed by some 

 recent experiments by Hurley and Spector (1961) at University 

 College Hospital. Small amounts of histamine injected intraderm- 

 ally into rats under conditions of rigid sterility are followed almost 

 immediately by increased capillary permeability to protein which 

 lasts for about 20 minutes. Sections of skin examined at this time 



