Abrogation of genetically controlled resistance of mice to Treponema pallidum by irradiation.
Infection with Treponema pallidum, the causative agent of human syphilis, gives rise to a complex immune response involving both humoral and cellular components. The exact nature of this response and how it relates to the disease process is a matter of considerable speculation. In recent years, studies have been directed towards defining the role of cell-mediated immunity (CMI) in syphilis. These have been conducted mainly in vitro because the general unavailability of inbred rabbits, the principal animals for experimental syphilis research, has limited the application of in vivo procedures. A prime deterrent to using mice for the study of syphilis has been their failure to exhibit pathology, even in the face of a persistent infection. We report here that on intradermal (i.d.) infection, transient primary lesions, characteristic of those seen in naturally acquired human syphilis, can be produced regularly in some strains of mice but not others, indicating a genetic basis for host susceptibility. Strains of mice which normally fail to develop lesions, do so after exposure to ionising radiation. Evidence is presented for a multiple role of the immune response during local infection.
D000818:Animals; D004195:Disease Models, Animal; D007109:Immunity / Q000528:radiation effects*; D007111:Immunity, Cellular / Q000528:radiation effects; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D013154:Spleen / Q000276:immunology; D013587:Syphilis / Q000276:immunology* / Q000473:pathology; D014210:Treponema pallidum