Protective efficacy of major outer membrane protein-specific immunoglobulin A (IgA) and IgG monoclonal antibodies in a murine model of Chlamydia trachomatis genital tract infection.

1995 ◽  
Vol 63 (12) ◽  
pp. 4704-4714 ◽  
Author(s):  
T W Cotter ◽  
Q Meng ◽  
Z L Shen ◽  
Y X Zhang ◽  
H Su ◽  
...  
Vaccine ◽  
2011 ◽  
Vol 29 (35) ◽  
pp. 5994-6001 ◽  
Author(s):  
Marien I. de Jonge ◽  
Sander A.S. Keizer ◽  
Hicham M. el Moussaoui ◽  
Lieke van Dorsten ◽  
Rima Azzawi ◽  
...  

2006 ◽  
Vol 2006 ◽  
pp. 1-6
Author(s):  
Joseph M. Lyons ◽  
James I. Ito ◽  
Servaas A. Morré

Objective.The aim of this study was to determine if vaginal application of the immune response modifier imiquimod (Aldara cream, 3M Pharmaceuticals, St Paul, Minn) would alter the course and/or outcome of female genital tract infection with a human isolate ofChlamydia trachomatisin a murine model.Methods.Groups of CF-1 mice were treated with Aldara on three different schedules: (1) ongoing beginning 5 days prior to and continuing through day 5 of infection; (2) a single prophylactic dose 2 hours prior to infection; and (3) therapeutic from day 4 to day 14 of infection. Mice were infected vaginally with a serovar D strain ofC trachomatis, and monitored by culture to determine the level of shedding and duration of infection.Results.We observed a significant reduction in both duration of infection and the level of shedding during the acute phase in mice treated on an ongoing basis commencing 5 days prior to infection. There was no effect with respect to the other regimens.Conclusion.These results demonstrate that ongoing Aldara treatment has efficacy and may enhance local innate immunity which reduces the duration of subsequent infection with human isolates ofC trachomatisin a murine model of female genital tract infection.


1999 ◽  
Vol 67 (6) ◽  
pp. 3019-3025 ◽  
Author(s):  
Kyle H. Ramsey ◽  
Todd W. Cotter ◽  
Rena D. Salyer ◽  
Gurwattan S. Miranpuri ◽  
Michael A. Yanez ◽  
...  

ABSTRACT We sought to assess the degree of cross-protective immunity in a mouse model of chlamydial genital tract infection. Following resolution of genital infection with the mouse pneumonitis (MoPn) biovar ofChlamydia trachomatis, mice were challenged intravaginally with either MoPn or human serovar E or L2. The majority of animals previously infected with MoPn were solidly immune to challenge with either of the two human biovars. Surprisingly, approximately 50% of animals became reinfected when homologously challenged with MoPn, although the secondary infection yielded significantly lower numbers of the organism isolated over a shorter duration than in the primary infection. Primary infection with serovar E also protected against challenge with MoPn or serovar L2, although the degree of immune protection was lower than that resulting from primary infection with MoPn. Blast transformation and assessment of delayed-type hypersensitivity indicated that mice previously infected with either human or murine biovars produced broadly cross-reactive T cells that recognized epitopes of either murine or human biovars of C. trachomatis. Immunoblotting demonstrated that primary MoPn infection produced immunoglobulin G (IgG) antibody to antigens of MoPn as well as at least three distinct antigenic components of human serovar E, one of which was identical in molecular weight to the major outer membrane protein (MOMP). Primary infection with serovar E produced IgG antibody reactive against serovar E but not MoPn MOMP and against at least one ca. 60-kDa protein of both chlamydial strains. Our results indicate that primary genital infection of mice with murineC. trachomatis induces immunity against challenge with either of two human biovars.


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