Chlamydia trachomatis infection of the male genital tract: what seems to be the trouble?

Chlamydia trachomatis is an intracellular pathogen that infects mucosal epithelial cells, causing persistent infections. Although chronic inflammation is a hallmark of chlamydial disease, the proinflammatory mechanisms involved are poorly understood. Little is known about how innate immunity in the male genital tract (MGT) responds to C. trachomatis. Toll-like receptors (TLRs) are a family of receptors of the innate immunity that recognize different pathogen-associated molecular patterns (PAMPs) present in bacteria, viruses, yeasts and parasites. The study of TLR expression in the MGT has been poorly investigated. The aim of this work was to investigate the keratinocyte-derived chemokine (KC) response of MGT primary cultures from C57BL/6 mice to C. trachomatis and different PAMPs. KC production by prostate, seminal vesicle and epididymis/vas deferens cell cultures was determined by ELISA in culture supernatants. TLR2, 3, 4 and 9 agonists induced the production of KC by all MGT primary cultures assayed. In addition, we analysed the host response against C. trachomatis and Chlamydia muridarum. Chlamydial LPS (cLPS) as well as C. trachomatis and C. muridarum infection induced KC secretion by all MGT cell cultures analysed. Differences in KC levels were observed between cultures, suggesting specific sensitivity against pathogens among MGT tissues. Chemokine secretion was observed after stimulation of seminal vesicle cells with TLR agonists, cLPS and C. trachomatis. To our knowledge, this is the first report showing KC production by seminal vesicle cells after stimulation with TLR ligands, C. trachomatis or C. muridarum antigens. These results indicate that different receptors of the innate immunity are present in the MGT. Understanding specific immune responses, both innate and adaptive, against chlamydial infections, mounted in each tissue of the MGT, will be crucial to design new therapeutic approaches where innate and/or adaptive immunity would be targeted.

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Interaction of Chlamydia trachomatis serovar E with male genital tract epithelium results in secretion of proinflammatory cytokines

Journal of Medical Microbiology ◽

10.1099/jmm.0.47241-0 ◽

2007 ◽

Vol 56 (8) ◽

pp. 1025-1032 ◽

Cited By ~ 26

Author(s):

Najwa Al-Mously ◽

Adrian Eley

Keyword(s):

Chlamydia Trachomatis ◽

Epithelial Cells ◽

Hela Cells ◽

Genital Tract ◽

Interleukin 1 ◽

Female Genital Tract ◽

Male Genital Tract ◽

Prostate Epithelial Cells ◽

Male Genital

Although much has been reported on the in vitro interaction of Chlamydia trachomatis with cells derived from the female genital tract, little is known of its interaction with male genital tract epithelium. The aim of this work was to investigate the effect of C. trachomatis serovar E on immortalized normal human urethral epithelial cells and on immortalized normal adult human prostate epithelial cells with regard to chlamydial growth and secretion of cytokines. After infection, these epithelial cells were assessed for their support of chlamydial growth in comparison with HeLa cells, and cytokine levels in cell culture supernatants were determined by ELISA. Although the male-derived epithelial cells supported growth of chlamydiae, the best growth was seen in HeLa cells. In contrast to prostate epithelial cells, the urethral epithelial cells released much larger quantities of interleukin 1α (IL-1α) following infection, whereas both IL-6 and IL-8 were produced in larger quantities by infected prostate cells. At 7 days post-infection, HeLa cells consistently produced large quantities of all three cytokines. In conclusion, the male-derived cell lines were shown to support the invasion of C. trachomatis and initiate a proinflammatory response to infection. From in vitro studies the suggestion that high levels of IL-6 could be a possible marker for chlamydial prostatitis is confirmed. Although not as marked a change, it is also suggested that higher IL-8 levels could be associated more with infection of the prostate than the urethra. Differential cytokine production by different male-derived epithelial cells could help determine the site of chlamydial infection and help in the study of pathogenesis.

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Male genital tract immune response against Chlamydia trachomatis infection

Reproduction ◽

10.1530/rep-16-0561 ◽

2017 ◽

Vol 154 (4) ◽

pp. R99-R110 ◽

Cited By ~ 1

Author(s):

Juan Pablo Mackern-Oberti ◽

Rubén Darío Motrich ◽

Maria Teresa Damiani ◽

Héctor Alex Saka ◽

Cristian Andrés Quintero ◽

...

Keyword(s):

Immune Response ◽

Chlamydia Trachomatis ◽

Epithelial Cells ◽

Genital Tract ◽

Host Immune Response ◽

Innate Immune ◽

T Helper ◽

Male Genital Tract ◽

Tract Infections ◽

Male Genital

Chlamydia trachomatisis the most commonly reported agent of sexually transmitted bacterial infections worldwide. This pathogen frequently leads to persistent, long-term, subclinical infections, which in turn may cause severe pathology in susceptible hosts. This is in part due to the strategies thatChlamydia trachomatisuses to survive within epithelial cells and to evade the host immune response, such as subverting intracellular trafficking, interfering signaling pathways and preventing apoptosis. Innate immune receptors such as toll-like receptors expressed on epithelial and immune cells in the genital tract mediate the recognition of chlamydial molecular patterns. After bacterial recognition, a subset of pro-inflammatory cytokines and chemokines are continuously released by epithelial cells. The innate immune response is followed by the initiation of the adaptive response againstChlamydia trachomatis, which in turn may result in T helper 1-mediated protection or in T helper 2-mediated immunopathology. Understanding the molecular mechanisms developed byChlamydia trachomatisto avoid killing and host immune response would be crucial for designing new therapeutic approaches and developing protective vaccines. In this review, we focus on chlamydial survival strategies and the elicited immune responses in male genital tract infections.

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