Update on the impact of Chlamydia trachomatis infection on male fertility

Andrologia ◽  
2004 ◽  
Vol 36 (1) ◽  
pp. 1-23 ◽  
Author(s):  
G. F. Gonzales ◽  
G. Munoz ◽  
R. Sanchez ◽  
R. Henkel ◽  
G. Gallegos-Avila ◽  
...  
2017 ◽  
Vol 29 (5) ◽  
pp. 466-473 ◽  
Author(s):  
M Moazenchi ◽  
M Totonchi ◽  
R Salman Yazdi ◽  
K Hratian ◽  
MA Mohseni Meybodi ◽  
...  

Chlamydia trachomatis (CT), an obligate intracellular bacterium, requires living cells to replicate. Half of men infected with CT are asymptomatic. CT infection can persist for up to four years within couples and affect their fertility. Chlamydia infection in men acts as a reservoir for transmission to women and can cause urinary tract inflammation, sperm DNA damage, and acute epididymitis. Semen samples from 1080 subfertile patients with normal and abnormal spermograms were examined to detect the presence of CT. An ELISA test was used to detect the presence of anti-CT IgA in these patients’ seminal plasma. CT infection was also confirmed by molecular investigation using specific primers. In order to evaluate the effect of CT infections on the DNA Fragmentation Index (DFI), 40 CT-infected cases and 20 CT-negative controls were analyzed by a Sperm Chromatin Structure Assay using flow cytometry. Among 1080 patients with poor sperm parameters, 155 (14.3%) patients were diagnosed with CT, 11% among those with semen abnormalities and 26% among those without semen abnormalities patients. The DFI was statistically higher in cases than in controls (p < 0.05). Given the prevalence of infection and also the high frequency of asymptomatic CT infection among infertile individuals with poor sperm parameters, screening for infection in these patients is essential in order to avoid adverse sequelae. We propose that the higher rate of DFI in CT-infected infertile men might be an underlying cause of their infertility and this warrants greater attention.


mBio ◽  
2019 ◽  
Vol 10 (4) ◽  
Author(s):  
Vonetta L. Edwards ◽  
Steven B. Smith ◽  
Elias J. McComb ◽  
Jeanne Tamarelle ◽  
Bing Ma ◽  
...  

ABSTRACT The mechanism(s) by which Lactobacillus-dominated cervicovaginal microbiota provide a barrier to Chlamydia trachomatis infection remain(s) unknown. Here we evaluate the impact of different Lactobacillus spp. identified via culture-independent metataxonomic analysis of C. trachomatis-infected women on C. trachomatis infection in a three-dimensional (3D) cervical epithelium model. Lactobacillus spp. that specifically produce d(−) lactic acid were associated with long-term protection against C. trachomatis infection, consistent with reduced protection associated with Lactobacillus iners, which does not produce this isoform, and with decreased epithelial cell proliferation, consistent with the observed prolonged protective effect. Transcriptomic analysis revealed that epigenetic modifications involving histone deacetylase-controlled pathways are integral to the cross talk between host and microbiota. These results highlight a fundamental mechanism whereby the cervicovaginal microbiota modulates host functions to protect against C. trachomatis infection. IMPORTANCE The vaginal microbiota is believed to protect women against Chlamydia trachomatis, the etiologic agent of the most prevalent sexually transmitted infection (STI) in developed countries. The mechanism underlying this protection has remained elusive. Here, we reveal the comprehensive strategy by which the cervicovaginal microbiota modulates host functions to protect against chlamydial infection, thereby providing a novel conceptual mechanistic understanding. Major implications of this work are that (i) the impact of the vaginal microbiota on the epithelium should be considered in future studies of chlamydial infection and other STIs and (ii) a fundamental understanding of the cervicovaginal microbiota’s role in protection against STIs may enable the development of novel microbiome-based therapeutic strategies to protect women from infection and improve vaginal and cervical health.


2019 ◽  
Vol 221 (4) ◽  
pp. 627-635 ◽  
Author(s):  
Jeanne Tamarelle ◽  
Bing Ma ◽  
Pawel Gajer ◽  
Mike S Humphrys ◽  
Mishka Terplan ◽  
...  

Abstract We characterized the composition and structure of the vaginal microbiota in a cohort of 149 women with genital Chlamydia trachomatis infection at baseline who were followed quarterly for 9 months after antibiotic treatment. At time of diagnosis, the vaginal microbiota was dominated by Lactobacillus iners or a diverse array of bacterial vaginosis–associated bacteria including Gardnerella vaginalis. Interestingly, L. iners–dominated communities were most common after azithromycin treatment (1 g monodose), consistent with the observed relative resistance of L. iners to azithromycin. Lactobacillus iners–dominated communities have been associated with increased risk of C. trachomatis infection, suggesting that the impact of antibiotic treatment on the vaginal microbiota could favor reinfections. These results provide support for the dual need to account for the potential perturbing effect(s) of antibiotic treatment on the vaginal microbiota, and to develop strategies to protect and restore optimal vaginal microbiota.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 740-740
Author(s):  
Gerard Karsenty

Abstract We hypothesized that bone may secrete hormones that regulate energy metabolism and reproduction. Testing this hypothesis revealed that the osteoblast-specific secreted protein osteocalcin is a hormone regulating glucose homeostasis and male fertility by signaling through a GPCR, Gprc6a, expressed in pancreatic β bells and Leydig cells of the testes. The systematic exploration of osteocalcin biology, revealed that it regulates an unexpectedly large spectrum of physiological functions in the brain and peripheral organs and that it has most features of an antigeromic molecule. As will be presented at the meeting, this body of work suggests that harnessing osteocalcin for therapeutic purposes may be beneficial in the treatment of age-related diseases such as depression, age-related memory loss and the decline in muscle function seen in sarcopenia.


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