Testosterone and other gonadal factor(s) restrict the efficacy of genes controlling resistance to Plasmodium chabaudi malaria

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Abstract
Summary The effect of circulating concentrations of testosterone (Te) on resistance to Plasmodium chabaudi malaria was investigated in the H‐2 congenic mouse strains C57BL/1, B10.A. 10.A(3R). B10.A(4R), and B10.D2. Te‐levels were determined by radioimmunoassay and resistance was expressed in terms of percent self‐healers after challenge with 106P. chabaudi‐infected erythrocytes. Our data indicate: (i) Females and castrated males reveal very similar interstrain variations of resistance. These do not correlate with the interstrain variations of the Te‐levels. This is consistent with the view that resistance to P. chaubaudi is controlled by genes of the H‐2 complex and genes of the non‐H‐2 B10‐background, (ii) The polygenic control of resistance is inefficacious at high Te‐levels. This is evident as high susceptibilities of males, Te‐treated females and Te‐treated castrated males. Moreover, high Te‐levels correlate with susceptibilities to P. chabaudi within mice of the same sex of a given strain, (iii) BlO‐males chemically castrated using buserdin display the same low Te‐leveel as those surgically castrated. The latter become resistant, while the former remain as highly susceptible to P. chabaudi is untreated B10‐males. Obviously, other gonadal factor(s), besides Te, impose restrictions on genes controlling resistance to P. chabaudi malaria.