The protective effects of the hormones androstenediol (androstene-3, 17,-diol; AED) and dehydroepiandrosterone (5-androsten-3-ol-17-one; DHEA) on the pathophysiology of two lethal bacterial infections and endotoxin shock were examined. The infections included a gram-positive organism () and a gram-negative organism (). Both hormones protected mice from the lethal bacterial infections and from lipopolysaccharide (LPS) challenge. Treatment of animals lethally infected with with DHEA resulted in a 43% protection whereas treatment with AED gave a 67% protection. Both hormones also protected completely animals infected with an LD50 dose of . Similarly, the 88% mortality rate seen in LPS challenge was reduced to 17% and 8.5%, by treatment with DHEA and AED, respectively. The protective influences of both steroids were shown not to be directly antibacterial, but primarily an indirect antitoxin reaction. DHEA appears to mediate its protective effect by a mechanism that blocks the toxin-induced production of pathopysiological levels of tumour necrosis factor- (TNF-) and interleukin-1. AED usually had greater protective effects than DHEA; however, the AED effect was independent of TNF- suppression, both and . The data suggest that both DHEA and AED may have a role in the neuro-endocrine regulation of antibacterial immune resistance.


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