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The Journal of Immunology, 1976, 117: 197-207.
Copyright © 1976 by The American Association of Immunologists, Inc.

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Humoral Immunity in Experimental Syphilis

II. The Relationship of Neutralizing Factors in Immune Serum to Acquired Resistance1,2,

Nancy H. Bishop3 and James N. Miller

From the Department of Microbiology and Immunology, School of Medicine, University of California, Los Angeles, California 90024

Abstract

Evidence for a humoral mechanism in immunity to experimental syphilis was provided by the demonstration of immune rabbit serum factor(s) capable of inactivating virulent Treponema pallidum, Nichols strain, in an in vitro-in vivo neutralization test. After intratesticular infection, rabbits were bled periodically and their resistance to reinfection was determined by challenge with T. pallidum. The results of challenge showed that resistance to reinfection begins to develop by 11 days after infection, becomes complete by 3 months, and persists for at least 2 years. In the neutralization test, a mixture of treponemal suspension and serum from the infected animals was incubated anaerobically at 34°C and the virulence of the treponemes was determined by intradermal inoculation into normal rabbits. Complete inactivation of treponemes by immune serum required heat-stable and heat-labile (56°C, 30 min) serum components and 16 hr of incubation, and was accelerated by pre-incubation of the treponemes for 4 hr with nonimmune serum but not by 100 µg/ml of added lysozyme. Serum-neutralizing activity, first demonstrable 1 month postinfection, was quantitated by a neutralizing endpoint (NEP). A relatively close quantitative correlation was shown between the development of resistance to symptomatic reinfection and the appearance and persistence of both TPI antibody and neutralizing serum factor(s). The nature of the serum factor(s), the mechanism of treponemal inactivation, and the application of the test in assessing the immune status are discussed.

Footnotes

1 This research was supported by Contracts N00014-69-A-0200-4039; NR 136-912 from the Office of Naval Research, 21-74-503 from the Center for Disease Control, United States Public Health Service, V3-181-26 from the World Health Organization, and Grant AI 12601-01 from the National Institutes of Health.

2 This work was presented in part at the 73rd Annual Meeting of the American Society for Microbiology, Miami, Florida, May 10, 1973.

3 In partial fulfillment of the requirements for the Doctor of Philosophy degree, University of California, Los Angeles. Predoctoral trainee supported by Training Grant AI 00249 from the United States Public Health Service.




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