Despite being the most common bacterial sexually transmitted infection worldwide, with 127 million new infections per year, a Chlamydia vaccine remains elusive. Vaccination remains the most highly recommended method for eliminating chlamydial transmission and subsequent pathology, the most severe of which is infertility. Research has predominantly focused on females even though a similar incidence of infection occurs in both sexes, resulting in potential vaccine candidates being trialled only in females. Male infections are often underappreciated as the effects on male fertility are still being defined. Some data suggests that Chlamydia causes sperm DNA fragmentation, which is an important clinical indicator of fertility.
We developed a male mouse model of prophylactic chlamydial vaccination. Male C57BL/6 mice were vaccinated intra-nasally with major outer membrane protein combined with Iscomatrix adjuvant (MOMP/IMX) or with IMX only, then challenged via the intra-penile route with Chlamydia muridarum, or PBS. At 1-, 2-, and 3-months post challenge the IMX adjuvant-only group had poor sperm quality demonstrated by lowered motility and oocyte-binding, abnormal morphology, and increased DNA damage. However, the MOMP/IMX vaccination group had comparable sperm quality to the non-infected control mice. Vaccination protected against infection-induced impairment of sperm motility, morphology, oocyte-binding, and DNA damage. Testicular and epididymal chlamydial burden were also reduced by vaccination. We hypothesise that vaccine-mediated protection is induced by CD4+ T cell involvement in both lower reproductive tract and testes, possibly combined with local IgA production.