256 /. /. Christian 



cytosis may be stimulated (Gordon and Katsh, 1949; Thomas, 1953). By 

 these several mechanisms the production of antibodies may be seriously 

 impaired following activation of the adrenal cortex although there appears 

 to be a dose-response relationship (Dougherty, 1953; Dougherty and 

 Schneebeli, 1955). While most of these effects were demonstrated most 

 clearly by injecting adrenocortical hormones, the same effects have been 

 shown repeatedly following stimulation of adrenocortical secretion in the 

 intact animal. 



d. Resistance to infection. The three immediately preceding topics all 

 deal with factors involved in the resistance to infection. It stands to reason 

 that reducing the inflammatory response to, and depressing the formation 

 of antibodies against, infectious agents will inevitably impair the ability of 

 an animal to resist infection. Cortisone, hydrocortisone, and ACTH have 

 been shown to decrease resistance to a variety of experimental infections 

 caused by a variety of infectious agents including streptococcal, pneumo- 

 coccal, tuberculosis infections in mice, rats, and guinea pigs, brucellosis, 

 malaria in monkeys, and others (Kligman etal., 1951 ; Schmidt and Squires, 

 1951 ; Selye, 1951 ; Kass et al., 1953b; Le Maistre et al., 1953; Robinson and 

 Smith, 1953). The pathogenicity of various agents has been increased by 

 cortisone injection. For example, the virulence of Coxsackie infections in 

 mice was greatly enhanced by cortisone (Boring et al., 1955), and polio- 

 myelitis can be made a paralytic disease in the normally resistant hamster 

 by cortisone or hydrocortisone (Shwartzman and Aronson, 1953). Vire- 

 mias may likewise be prolonged appreciably by the adrenal glucocorticoids 

 (Whitney and Anigstein, 1953; Pollard and Wilson, 1955). The list of 

 experimental infections which have been made more virulent, prolonged, 

 or otherwise increased in their pathogenicity by treatment with carbohy- 

 drate-active adrenocorticoids or ACTH (Selye, 1951) is long, and there is 

 no point in listing them in detail here. 



Whenever experiments with injected hormones are considered the ques- 

 tion arises whether or not the same events may occur as a result of in- 

 creased endogenous secretion of the same or similar hormones. A criticism 

 frequently made of experiments with exogenous hormones, especially with 

 large doses, is that the results are pharmacologic rather than physiologic. 

 However, it is by using isolated hormones in highly controlled situations 

 that an understanding of the basic mechanisms is gained. Nevertheless, 

 before one can extrapolate from these data to natural events, comparable 

 changes must be shown to occur in natural or seminatural conditions. 

 Changes in host resistance may result from adverse environmental stimuli, 

 possibly as a result of adrenocortical activity. It has long been common 

 knowledge that excess fatigue, chilling, and a variety of comparable stimuli 

 increase the susceptibility of humans to colds and other infections. It should 



