The Effectiveness of Tuberculo-Glycolipid as an Adjuvant in Eliciting Allergic Encephalomyelitis and Aspermatogenesis

Guinea pigs were injected with testicular extract incorporated in water-in-oil emulsion containing graded amounts of killed, dried Mycobacterium tuberculosis or Wax D from human type of tubercle bacilli. The minimum amount of tubercle bacilli required to induce aspermatogenesis was 0.015 mg; and of Wax D, 0.1 mg. Guinea pigs were injected with rabbit spinal cord incorporated in water-in-oil emulsion containing graded amounts of killed, dried M. tuberculosis or Wax D from human strain tubercle bacilli. The minimum amount of tubercle bacilli required to induce encephalomyelitis with death was 0.04 mg; and of Wax D, 0.4 mg. The minimum amount of tubercle bacilli which induces encephalomyelitis with recovery was 0.02 mg; and of Wax D, 0.2 mg. The guinea pigs were tested for tuberculin sensitization. The minimum amount of tubercle bacilli or Wax D in the water-in-oil emulsion required for sensitization was determined: 0.0004 mg for M. tuberculosis, and 0.2 mg for Wax D. The data summarized in paragraphs 1 and 2 above indicate that 7–10 times more Wax D than tubercle bacilli was required for inducing allergic encephalomyelitis and aspermatogenesis. Since Wax D is only 6–8% of the whole bacillus, it may be concluded that if Wax D is the active factor in inducing delayed hypersensitivity, it is 84–160 times more active when contained in the mycobacterium than after isolation and purification. This consideration is not in favor of, but does not exclude, the role of Wax D in eliciting hypersensitivity of the delayed type. Various interpretations are discussed.