期刊
VACCINES
卷 11, 期 3, 页码 -出版社
MDPI
DOI: 10.3390/vaccines11030504
关键词
Chlamydia muridarum; vaccine; mouse; major outer membrane protein; polymorphic membrane protein G; plasmid glycoprotein 3; adjuvants
Chlamydia trachomatis is a common sexually transmitted pathogen, and a safer and more effective vaccine is urgently needed. This study found that the antigens PmpG and Pgp3, alone or in combination with MOMP, elicited weaker immune responses, while vaccination with MOMP induced a robust immune response and protected against a respiratory challenge with C. muridarum. Pgp3 antagonized the protection induced by MOMP.
Chlamydia trachomatis is the most common bacterial sexually transmitted pathogen. The number of chlamydial infections continuous to increase and there is an urgent need for a safe and efficacious vaccine. To assess the ability of the Chlamydia muridarum polymorphic membrane protein G (PmpG) and the plasmid glycoprotein 3 (Pgp3) as single antigens, and in combination with the major outer-membrane protein (MOMP) to induce protection, BALB/c mice were immunized utilizing CpG-1826 and Montanide ISA 720 VG as adjuvants. Following vaccination with MOMP, significant humoral and cell-mediated immune responses were observed, while immunization with PmpG, or Pgp3, elicited weaker immune responses. Weaker immune responses were induced with MOMP+Pgp3 compared with MOMP alone. Following the intranasal challenge with C. muridarum, mice vaccinated with MOMP showed robust protection against body-weight loss, inflammatory responses in the lungs and number of Chlamydia recovered from the lungs. PmpG and Pgp3 elicited weaker protective responses. Mice immunized with MOMP+PmpG, were no better protected than animals vaccinated with MOMP only, while Pgp3 antagonized the protection elicited by MOMP. In conclusion, PmpG and Pgp3 elicited limited protective immune responses in mice against a respiratory challenge with C. muridarum and failed to enhance the protection induced by MOMP alone. The virulence of Pgp3 may result from its antagonistic effect on the immune protection induced by MOMP.
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