| Summary: | <p>Abstract</p> <p>Background</p> <p><it>Chlamydia pneumoniae</it> is an obligate intracellular respiratory pathogen for humans. Infection by <it>C. pneumoniae</it> may be linked etiologically to extra-respiratory diseases of aging, especially atherosclerosis. We have previously shown that age promotes <it>C. pneumoniae</it> respiratory infection and extra-respiratory spread in BALB/c mice.</p> <p>Findings</p> <p>Aged C57BL/6 mice had a greater propensity to develop chronic and/or progressive respiratory infections following experimental intranasal infection by <it>Chlamydia pneumoniae</it> when compared to young counterparts. A heptavalent CTL epitope minigene (CpnCTL7) vaccine conferred equal protection in the lungs of both aged and young mice. This vaccine was partially effective in protecting against <it>C. pneumoniae</it> spread to the cardiovascular system of young mice, but failed to provide cardiovascular protection in aged animals.</p> <p>Conclusions</p> <p>Our findings suggest that vaccine strategies that target the generation of a <it>C. pneumoniae</it>-specific CTL response can protect the respiratory system of both young and aged animals, but may not be adequate to prevent dissemination of <it>C. pneumoniae</it> to the cardiovascular system or control replication in those tissues in aged animals.</p>
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