<em>Chlamydia muridarum</em> Infection-Induced Destruction of Murine Male Germ Cells and Sertoli Cells is Partly Prevented by <em>Chlamydia</em> Major Outer Membrane Protein-Specific Non IFNγ-secreting CD4 cells — ASN Events
  1. Schedule
  2. Poster Session 2-Spermatology
  3. Chlamydia muridarum Infection-Induced Destruction of Murine Male Germ Cells and Sertoli Cells is Partly Prevented by Chlamydia Major Outer Membrane Protein-Specific Non IFNγ-secreting CD4 cells

Chlamydia muridarum Infection-Induced Destruction of Murine Male Germ Cells and Sertoli Cells is Partly Prevented by Chlamydia Major Outer Membrane Protein-Specific Non IFNγ-secreting CD4 cells (#203)

Kate A Redgrove 1 , Alexander Sobinoff 1 , Samantha Dando 2 , Jessie M Sutherland 1 , Charles W Armitage 2 , Peter Timms 2 , Eileen McLaughlin 1 , Kenneth W Beagley 2
  1. 1. Priority Research Centres in Chemical Biology and Reproductive Science, University of Newcastle, Callaghan, NSW, Australia
  2. 2. Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia

Chlamydia trachomatis is the most common sexually transmitted disease worldwide, where it is estimated that more than 100 million new cases are reported annually. While there have been extensive studies into the adverse effects that Chlamydia infection has on the female reproduction, studies into the consequences on male fertility have been limited and controversial. This is in part due to the asymptomatic nature of the infection, withapproximately 50% of men with Chlamydia failing to show symptoms. It is accepted however, that acute and/or persistent Chlamydia infection is the causative agent for conditions that can potentiallyimpact on male fertility, including urethritis, epididymitis and orchitis: however the role of Chlamydia in prostatitis and male factor infertility remains controversial. Using a mouse model of C. muridarum infection in male C57BL/6 mice, we investigated the effects of chlamydial infection on spermatogenesis and determined the potential of immune T cells to prevent infection-induced outcomes. Infection disrupted seminiferous tubules causing loss of germ cells at 4 and 8 weeks post infection, with the most severely affected tubules containing only Sertoli cells. Increased mitotic proliferation, DNA repair and apoptosis in spermatogonial cells and damaged germ cells were evident in atrophic tubules. Caspase 3 staining revealed increased (6-fold) numbers of Sertoli cells with abnormal morphology in the seminiferous tubules of infected mice indicating significant levels of apoptosis. Sperm count and motility were both decreased in infected mice and there was a significant decrease in morphologically normal spermatozoa. Interestingly, adoptive transfer of immune CD4 cells, particularly Th2-like cells prior to infection prevented these effects on spermatogenesis and Sertoli cells. Furthermore, immune T cells significantly reduced the infectious burden in the penile urethra, epididymis and Vas deferens. These data suggest that chlamydial infection adversely affects spermatogenesis and male fertility and that vaccination can potentially prevent the spread of infection and these adverse outcomes.