TY - JOUR
T1 - Induction of protective immunity against Chlamydia muridarum intracervical infection in DBA/1j mice
AU - Tang, Lingli
AU - Yang, Zhangsheng
AU - Zhang, Hongbo
AU - Zhou, Zhiguang
AU - Arulanandam, Bernard
AU - Baseman, Joel
AU - Zhong, Guangming
N1 - Funding Information:
This work was supported in part by grants (to G. Zhong) from the US National Institutes of Health .
PY - 2014/3/10
Y1 - 2014/3/10
N2 - We previously reported that intracervical inoculation with Chlamydia muridarum induced hydrosalpinx in DBA/1j mice, but intravaginal inoculation failed to do so. In the current study, we found unexpectedly that intrabursal inoculation of live chlamydial organisms via the oviduct failed to induce significant hydrosalpinx. We further tested whether primary infection via intravaginal or intrabursal inoculation could induce protective immunity against hydrosalpinx following intracervical challenge infection. Mice infected intravaginally with C. muridarum were fully protected from developing hydrosalpinx, while intrabursal inoculation offered partial protection. We then compared immune responses induced by the two genital tract inoculations. Both inoculations induced high IFNγ and IL-17 T cell responses although the ratio of IgG2a versus IgG1 in intravaginally infected mice was significantly higher than in mice infected intrabursally. When the antigen-specificities of antibody responses were compared, both groups of mice dominantly recognized 24 C. muridarum antigens, while each group preferentially recognized unique sets of antigens. Thus, we have demonstrated that intrabursal inoculation is neither effective for causing hydrosalpinx nor efficient in inducing protective immunity in DBA/1j mice. Intravaginal immunization, in combination with intracervical challenge infection in DBA/1j mice, can be a useful model for understanding mechanisms of chlamydial pathogenicity and protective immunity.
AB - We previously reported that intracervical inoculation with Chlamydia muridarum induced hydrosalpinx in DBA/1j mice, but intravaginal inoculation failed to do so. In the current study, we found unexpectedly that intrabursal inoculation of live chlamydial organisms via the oviduct failed to induce significant hydrosalpinx. We further tested whether primary infection via intravaginal or intrabursal inoculation could induce protective immunity against hydrosalpinx following intracervical challenge infection. Mice infected intravaginally with C. muridarum were fully protected from developing hydrosalpinx, while intrabursal inoculation offered partial protection. We then compared immune responses induced by the two genital tract inoculations. Both inoculations induced high IFNγ and IL-17 T cell responses although the ratio of IgG2a versus IgG1 in intravaginally infected mice was significantly higher than in mice infected intrabursally. When the antigen-specificities of antibody responses were compared, both groups of mice dominantly recognized 24 C. muridarum antigens, while each group preferentially recognized unique sets of antigens. Thus, we have demonstrated that intrabursal inoculation is neither effective for causing hydrosalpinx nor efficient in inducing protective immunity in DBA/1j mice. Intravaginal immunization, in combination with intracervical challenge infection in DBA/1j mice, can be a useful model for understanding mechanisms of chlamydial pathogenicity and protective immunity.
KW - Chlamydia muridarum
KW - DBA/1J
KW - Intrabursal
KW - Intracervical infection
KW - Intravaginal
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U2 - 10.1016/j.vaccine.2013.10.018
DO - 10.1016/j.vaccine.2013.10.018
M3 - Article
C2 - 24188757
AN - SCOPUS:84894454995
SN - 0264-410X
VL - 32
SP - 1407
EP - 1413
JO - Vaccine
JF - Vaccine
IS - 12
ER -