https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14037 Wed 11 Apr 2018 16:17:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42488 Chlamydia infection, in both females and males, is increasing worldwide. Male infections have been associated clinically with urethritis, epididymitis, and orchitis, believed to be caused by ascending infection, although the impact of infection on male fertility remains controversial. Using a mouse model of male chlamydial infection, we show that all the major testicular cell populations, germ cells, Sertoli cells, Leydig cells, and testicular macrophages can be productively infected. Furthermore, sperm isolated from vas deferens of infected mice also had increased levels of DNA damage as early as 4 weeks post-infection. Bilateral vasectomy, prior to infection, did not affect the chlamydial load recovered from testes at 2, 4, and 8 weeks post-infection, and Chlamydia-infected macrophages were detectable in blood and the testes as soon as 3 days post-infection. Partial depletion of macrophages with clodronate liposomes significantly reduced the testicular chlamydial burden, consistent with a hematogenous route of infection, with Chlamydia transported to the testes in infected macrophages. These data suggest that macrophages serve as Trojan horses, transporting Chlamydia from the penile urethra to the testes within 3 days of infection, bypassing the entire male reproductive tract. In the testes, infected macrophages likely transfer infection to Leydig, Sertoli, and germ cells, causing sperm DNA damage and impaired spermatogenesis.]]> Tue 23 Aug 2022 15:34:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7711 Sat 24 Mar 2018 08:41:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7879 Sat 24 Mar 2018 08:41:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15982 -/- mice had reduced infection, inflammation, and mucus-secreting cell hyperplasia. Surprisingly, infection of wild-type (WT) mice did not increase IL-13 production but reduced IL-13Rα2 decoy receptor levels compared with sham-inoculated controls. Infection of WT but not Il13^-/- mice induced persistent AHR. Infection and associated pathology were restored in infected Il13^-/- mice by reconstitution with IL-13. Stat6^-/- mice were also largely protected. Neutralization of IL-13 during infection prevented subsequent infection-induced severe AAD. Thus, early-life Chlamydia respiratory infection reduces IL-13Rα2 production, which may enhance the effects of constitutive IL-13 and promote more severe infection, persistent AHR, and AAD.]]> Sat 24 Mar 2018 08:23:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9871 Sat 24 Mar 2018 08:12:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12215 Sat 24 Mar 2018 08:12:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22617 Sat 24 Mar 2018 07:12:43 AEDT ]]>