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Abstract Cortisone alters the development and resolution of experimental syphilitic lesions in the rabbit. Cortisone acetate was administered to separate groups of rabbits during the 1st, 2nd, or 4th wk after intratesticular infection with Treponema pallidum. Controls included uninfected rabbits given a similar cortisone treatment regimen as well as uninfected and infected rabbits not treated with cortisone. The development of humoral and cellular immunity was determined by measurement of serum antibody titers and antigen-induced in vitro histogenesis. Tissues obtained from these animals were examined by routine histologic methods and by immunofluorescent staining for T. pallidum, T lymphocytes, and immunoglobulin. Significant alterations in the kinetics of the immune response and the nature of cellular infiltration, bacterial clearance, and healing were observed after cortisone therapy. The administration of cortisone during the 1st wk of infection (inductive phase of immune response) results in delayed appearance of specific humoral and cellular immunity. Lymphocyte responsiveness to concanavalin A is unaffected by syphilitic infection and/or cortisone administration. After cessation of cortisone treatment, a rapid appearance of specific immune products occurs. Similarly, cellular infiltration and bacterial clearance are delayed, but proceed thereafter in a relatively normal fashion. Cortisone administration has a lesser effect on previously established humoral and cellular responses (effector phase of immune response): slight temporary reductions in antibody titer and specific blastogenic responses are observed when cortisone is given during the 2nd wk of infection. Effector activity at the local site of infection is diminished, however, and the steroid-treated animals display a decreased capacity to eliminate organisms effectively from the primary site. In the later lesions of cortisone-treated infected animals, the cytoplasm of numerous macrophages contains large amounts of treponemal antigen; these cells appear to be unable to digest the phagocytized bacteria as well as macrophages of control animals. Cortisone therapy during healing causes the temporary reversal of the fibrotic process and allows the reappearance of treponemes at the primary site. Immunologic mechanisms appear to be responsible for the initial bacterial clearance as well as the control of bacterial multiplication during early latency. We conclude that the course of experimental syphilis infection is determined largely by the host immune response.
Lukehart et al. (Thu,) studied this question.