- Title
- Chronic testicular Chlamydia muridarum infection impairs mouse fertility and offspring development
- Creator
- Bryan, Emily R.; Redgrove, Kate A.; Mooney, Alison R.; Mihalas, Bettina P.; Sutherland, Jessie M.; Carey, Alison J.; Armitage, Charles W.; Trim, Logan K.; Kollipara, Avinash; Mulvey, Peter B. M.; Palframan, Ella; Trollope, Gemma; Bogoevski, Kristofor; McLachlan, Robert; McLaughlin, Eileen A.; Beagley, Kenneth W.
- Relation
- NHMRC.1062198 http://purl.org/au-research/grants/nhmrc/1062198
- Relation
- Biology of Reproduction Vol. 102, Issue 4, p. 888-901
- Publisher Link
- http://dx.doi.org/10.1093/biolre/ioz229
- Publisher
- Oxford University Press
- Resource Type
- journal article
- Date
- 2020
- Description
- With approximately 131 million new genital tract infections occurring each year, Chlamydia is the most common sexually transmitted bacterial pathogen worldwide. Male and female infections occur at similar rates and both cause serious pathological sequelae. Despite this, the impact of chlamydial infection on male fertility has long been debated, and the effects of paternal chlamydial infection on offspring development are unknown. Using a male mouse chronic infection model, we show that chlamydial infection persists in the testes, adversely affecting the testicular environment. Infection increased leukocyte infiltration, disrupted the blood:testis barrier and reduced spermiogenic cell numbers and seminiferous tubule volume. Sperm from infected mice had decreased motility, increased abnormal morphology, decreased zona-binding capacity, and increased DNA damage. Serum anti-sperm antibodies were also increased. When both acutely and chronically infected male mice were bred with healthy female mice, 16.7% of pups displayed developmental abnormalities. Female offspring of chronically infected sires had smaller reproductive tracts than offspring of noninfected sires. The male pups of infected sires displayed delayed testicular development, with abnormalities in sperm vitality, motility, and sperm-oocyte binding evident at sexual maturity. These data suggest that chronic testicular Chlamydia infection can contribute to male infertility, which may have an intergenerational impact on sperm quality.
- Subject
- genital tract infections; sexually transmitted bacteria; sperm; male infertility
- Identifier
- http://hdl.handle.net/1959.13/1428193
- Identifier
- uon:38608
- Identifier
- ISSN:0006-3363
- Rights
- © The Author(s) 2020. Published by Oxford University Press on behalf of Society for the Study of Reproduction. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
- Language
- eng
- Full Text
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