PHAGOCYTOSIS 2Q3 



latter removed by washing, are readily ingested. The action, 

 therefore, must be on the serum i.e., aggressin must act as an 

 anti-opsonin. 



This leads us to Wassermann and Citron's explanation of the 

 phenomena. They suppose aggressins to be simply solutions of the 

 bacterial protoplasm which have the power of combining with the 

 specific protective substances of the animal, and so disarming its 

 methods of defence. In other words, they are solutions of endo- 

 toxin of feeble toxicity. This view is strongly supported indeed, 

 practically proved by the researches of Doerr, who found that 

 aggressins caused a precipitate when mixed with their specific 

 immune sera, and that their presence might bring about an 

 absorption of the complements, just as if they were free bacterial 

 receptors. There are a few minor differences between aggressins 

 prepared in vivo and those obtained from cultures in vitro, but 

 not more than we might expect from the differences in their mode 

 of production. 



If aggressins are merely free molecules of bacterial protoplasm, 

 we should expect them to combine with opsonins, just as do the 

 bacteria themselves, and hence to act as anti-opsonins. And this 

 supplies a striking proof of the specificity of the opsonins, for, as 

 already stated, an aggressin of one organism (e.g., B. coli) does 

 not prevent the phagocytosis of another organism (e.g., B. subtilis). 

 This must apply to the thermolabile opsonin, or opsonin proper, 

 since these experiments were made on normal animals. 



The relationship between virulence and phagocytosis is an 

 interesting one. As a general rule, it will be found, as shown by 

 the extensive researches of Metchnikoff and his school, that there 

 is an inverse ratio between the two : when an organism is viru- 

 lent for an animal it will be ingested by the leucocytes to a very 

 slight extent, and vice versa. This refers, of course, mainly to 

 natural immunity, since in acquired immunity other factors, such 

 as the action of bacteriolysins or antitoxins, may come in. There 

 are, however, some exceptions. Thus, tubercle bacilli injected 

 into the peritoneum of normal guinea-pigs are readily taken up by 

 the phagocytes. We must assume in this case that an organism 

 may be taken up whilst it is alive and uninjured, that it may be 

 entirely indigestible by the leucocyte, and may continue to grow 

 and multiply in its interior. This is also sometimes seen in acute 

 infections : the common localization of the meningococcus in the 

 polynuclear leucocytes is well known, and Andrewes has described 



