The mechanism(s) of resistance to treponemal infection has not been elucidated. We have shown that serum or T-cells obtained from inbred hamsters immune to Treponema pallidum Bosnia A or T. pertenue can confer protection on hamsters to challenge with the homologous strain. The objectives of the present proposal are to determine: (1) whether macrophages specifically (T cells) or nonspecifically activated can kill treponemes in the presence or absence of treponemal immune serum; (2) whether immune treponemal T-cells or their products can kill treponemes; (3) whether specific resistance to infection with T. pallidum or T. pertenue can be detected with whole or fractionated (IgM, IgG2 or IgG1) immune serum; (4) whether specific resistance can be conferred on recipients with B cells; (5) in vitro responses of syphilitic and frambesial T-cells to mitogens and treponemal antigens; (6) whether treponemal lymphocytes (T or B cells) or macrophages can impair the mitogenic responses of normal hamster lymphocytes; (7) the temporal relationship between the development and regression of treponemal lesions and infiltration of macrophages and T and B cells into these tissues. The cellular infiltration of the inguinal lymph nodes will also be examined since they teem with treponemes; and (8) whether T cells or immune serum from hamsters immune to T. pallidum Bosnia A, T. pallidum Nichols or T. pertenue can confer protection on recipients to challenge with the heterologous strain. Investigation of the mechanism of resistance by which hamsters respond to treponemal infection may delineate the mechanism by which humans respond to syphilitic or frambesial infection.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI022199-02
Application #
3133039
Study Section
Bacteriology and Mycology Subcommittee 1 (BM)
Project Start
1984-09-30
Project End
1987-08-31
Budget Start
1985-09-01
Budget End
1986-08-31
Support Year
2
Fiscal Year
1985
Total Cost
Indirect Cost
Name
University of Wisconsin Madison
Department
Type
Schools of Medicine
DUNS #
161202122
City
Madison
State
WI
Country
United States
Zip Code
53715
Lovrich, S D; Callister, S M; DuChateau, B K et al. (1995) Abilities of OspA proteins from different seroprotective groups of Borrelia burgdorferi to protect hamsters from infection. Infect Immun 63:2113-9
Lovrich, S D; Callister, S M; Lim, L C et al. (1994) Seroprotective groups of Lyme borreliosis spirochetes from North America and Europe. J Infect Dis 170:115-21
Lim, L C; England, D M; DuChateau, B K et al. (1994) Development of destructive arthritis in vaccinated hamsters challenged with Borrelia burgdorferi. Infect Immun 62:2825-33
Liu, Y F; Lim, L C; Schell, K et al. (1994) Differentiation of borreliacidal activity caused by immune serum or antimicrobial agents by flow cytometry. Clin Diagn Lab Immunol 1:145-9
Lim, L C; Liu, Y F; Schell, K et al. (1994) Detection of borreliacidal antibody by using acridine orange and flow cytometry. Clin Diagn Lab Immunol 1:44-50
Lovrich, S D; Callister, S M; Lim, L C et al. (1993) Seroprotective groups among isolates of Borrelia burgdorferi. Infect Immun 61:4367-74
Kenefick, K B; Lim, L C; Alder, J D et al. (1993) Induction of interleukin-1 release by high- and low-passage isolates of Borrelia burgdorferi. J Infect Dis 167:1086-92
Schmitz, J L; Schell, R F; Callister, S M et al. (1992) Immunoglobulin G2 confers protection against Borrelia burgdorferi infection in LSH hamsters. Infect Immun 60:2677-82
Kenefick, K B; Lederer, J A; Schell, R F et al. (1992) Borrelia burgdorferi stimulates release of interleukin-1 activity from bovine peripheral blood monocytes. Infect Immun 60:3630-4
Lovrich, S D; Callister, S M; Schmitz, J L et al. (1991) Borreliacidal activity of sera from hamsters infected with the Lyme disease spirochete. Infect Immun 59:2522-8

Showing the most recent 10 out of 20 publications