TY - JOUR
T1 - Chronic testicular Chlamydia muridarum infection impairs mouse fertility and offspring development†
AU - Bryan, Emily R.
AU - Redgrove, Kate A.
AU - Mooney, Alison R.
AU - Mihalas, Bettina P.
AU - Sutherland, Jessie M.
AU - Carey, Alison J.
AU - Armitage, Charles W.
AU - Trim, Logan K.
AU - Kollipara, Avinash
AU - Mulvey, Peter B.M.
AU - Palframan, Ella
AU - Trollope, Gemma
AU - Bogoevski, Kristofor
AU - McLachlan, Robert
AU - McLaughlin, Eileen A.
AU - Beagley, Kenneth W.
PY - 2020/4/15
Y1 - 2020/4/15
N2 - 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.
AB - 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.
KW - Chlamydia
KW - male infertility
KW - offspring development
KW - sperm DNA damage
KW - STI
UR - http://www.scopus.com/inward/record.url?scp=85083042586&partnerID=8YFLogxK
U2 - 10.1093/biolre/ioz229
DO - 10.1093/biolre/ioz229
M3 - Article
C2 - 31965142
SN - 0006-3363
VL - 102
SP - 888
EP - 901
JO - Biology of Reproduction
JF - Biology of Reproduction
IS - 4
ER -