Lack of humoral immune protection against Treponema denticola virulence ina murine model

This study investigated the characteristics of humoral immune responses to Treponema denticola following primary infection, reinfection, and active im munization, as well as immune protection in mice. Primary infection with T. denticola induced a significant (400-fold) serum immunoglobulin G (IgG) re sponse compared to that in control uninfected mice. The IgG response to rei nfection was 20,000-fold higher than that for control mice and 10-fold high er than that for primary infection. Mice actively immunized with formalin-k illed treponemes developed serum antibody levels seven- to eightfold greate r than those in animals after primary infection. Nevertheless, mice with th is acquired antibody following primary infection or active immunization dem onstrated no significant alterations of lesion induction or decreased size of the abscesses following a challenge infection, Mice with primary infecti on developed increased levels of IgG3, IgG2b, and IgG2a antibodies, with Ig G1 being lower than the other subclasses. Reinfected mice developed enhance d IgG2b, IgG2a, and IgG3 and less IgG1. In contrast, immunized mice develop ed higher IgG1 and lower IgG3 antibody responses to infection. These IgG su bclass distributions indicate a stimulation of both Th1 and Th2 activities in development of the humoral immune response to infection and immunization . Our findings also demonstrated a broad antigen reactivity of the serum an tibody, which was significantly increased with reinfection and active immun ization. Furthermore, serum antibody was effective in vitro in immobilizing and clumping the bacteria but did not inhibit growth or passively prevent the treponemal infection. These observations suggest that humoral immune re sponses, as manifested by antibody levels, isotype, and antigenic specifici ty, were not capable of resolving a T. denticola infection.