scholarly journals Resolution of Secondary Chlamydia trachomatis Genital Tract Infection in Immune Mice with Depletion of Both CD4+ and CD8+ T cells

2001 ◽  
Vol 69 (4) ◽  
pp. 2643-2649 ◽  
Author(s):  
Sandra G. Morrison ◽  
Richard P. Morrison

ABSTRACT The essential role of T cells in the resolution of primary murineChlamydia trachomatis genital tract infection is inarguable; however, much less is known about the mechanisms that confer resistance to reinfection. We previously established that CD4+ T cells and B cells contribute importantly to resistance to reinfection. In our current studies, we demonstrate that immune mice concurrently depleted of both CD4+ T cells and CD8+ T cells resisted reinfection as well as immunocompetent wild-type mice. The in vivo depletion of CD4+ and CD8+ T cells resulted in diminished chlamydia-specific delayed-type hypersensitivity responses, but antichlamydial antibody responses were unaffected. Our data indicate that immunity to chlamydial genital tract reinfection does not rely solely upon immune CD4+ or CD8+ T cells and further substantiate a predominant role for additional effector immune responses, such as B cells, in resistance to chlamydial genital tract reinfection.

2000 ◽  
Vol 68 (5) ◽  
pp. 2870-2879 ◽  
Author(s):  
Sandra G. Morrison ◽  
Richard P. Morrison

ABSTRACT Adaptive immune responses contribute to the resolution ofChlamydia trachomatis genital tract infection and protect against reinfection, but our understanding of the mechanisms of those protective responses is incomplete. In this study, we analyzed by in situ immunohistochemistry the progression of the inflammatory and cytokine responses in the genital tracts of mice vaginally infected with C. trachomatis strain mouse pneumonitis. The cellular inflammatory response was characterized by an initial elevation in myeloid cells in the vagina (day 3) and uterine horns (day 7), followed by a marked rise in the number of T cells, predominantly CD4+ cells. CD8+ T cells and CD45R+B cells were also detected but were much less numerous. Perivascular clusters of CD4+ T cells, which resembled clusters of T cells seen in delayed-type hypersensitivity responses, were evident by 2 weeks postinfection. Following the resolution of infection, few CD8+ T cells and CD45R+ B cells remained, whereas numerous CD4+ T cells and perivascular clusters of CD4+ T cells persisted in genital tract tissues. Interleukin-12 (IL-12)- and tumor necrosis factor alpha (TNF-α)-producing cells were observed in vaginal tissue by day 3 of infection and in uterine tissues by day 7. Cells producing IL-4 or IL-10 were absent from vaginal tissues at day 3 of infection but were present in uterine tissues by day 7 and were consistently more numerous than IL-12- and TNF-α-producing cells. Thus, the evolution of the local inflammatory response was characterized by the accumulation of CD4+ T cells into perivascular clusters and the presence of cells secreting both Th1- and Th2-type cytokines. The persistence of CD4+-T-cell clusters long after infection had resolved (day 70) may provide for a readily mobilizable T-cell response by which previously infected animals can quickly respond to and control a secondary infectious challenge.


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.


1999 ◽  
Vol 67 (10) ◽  
pp. 5518-5521 ◽  
Author(s):  
James I. Ito ◽  
Joseph M. Lyons

ABSTRACT Earlier investigations have not shown an important role for gamma interferon (IFN-γ) in the early clearance of chlamydial infection from the murine female genital tract. In a model using a human genital isolate of Chlamydia trachomatis in IFN-γ and IFN-γ receptor knockout mice, we were able to demonstrate a major role for IFN-γ in mediating control of infection throughout the course of infection.


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 ◽  
...  

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