The two-sided role of the vaginal microbiome in Chlamydia trachomatis and Mycoplasma genitalium pathogenesis

Abstract

Sexually transmitted infections (STI) can have major consequences for the reproductive health of women. Mycoplasma genitalium is a STI that is not as well studied but causes pelvic inflammatory disease (PID) among other complications. Another well-known STI is Chlamydia trachomatis, notorious for its capability to cause infertility. Both C. trachomatis and M. genitalium share some of the same clinical aspects. Parts of the pathogenesis of C. trachomatis and M. genitalium infections are unclear but potential factors are the microbiome and other STIs. The healthy vaginal microbiome is dominated by Lactobacillus spp; these bacteria protect the host against invading bacteria like C. trachomatis and M. genitalium by producing antibacterial compounds and providing a mechanical barrier. A dysbiosis of the vaginal microbiome is characterized by a non-Lactobacillus spp. dominated microbiome, also known as bacterial vaginosis (BV). BV and BV associated bacteria play a role in the pathogenesis of STIs such as C. trachomatis and M. genitalium. The different species of BV associated bacteria have distinct characteristics that could play a role in C. trachomatis and M. genitalium infections. Host factors should also be considered when analysing the interaction of C. trachomatis and M. genitalium and the microbiome. One important factor is the hormonal homeostasis. Oral hormonal contraception influences the vaginal milieu and could influence the infection process of STIs. Overall, this review attempts to give an overview of the pathogenesisof C. trachomatis and M. genitalium infections and the relationship between M. genitalium, C. trachomatis, and the vaginal microbiome.

The Complexity of Interactions Between Female Sex Hormones and Chlamydia trachomatis Infections

“…The role of the host vaginal microbiota is an understudied factor in the interactions with FSHs and Chlamydia. Studies have suggested that C. trachomatis infection is associated with altered diversity in the vaginal microbiome, as reviewed by Molenaar, et al and others [73,79]. In baboons, C. trachomatis infection in the presence of the LNG-IUS decreased the total number of microbiome-associated bacteria, but not the diversity of the vaginal microbiome [78].…”

The Interaction Between Microorganisms, Metabolites, and Immune System in the Female Genital Tract Microenvironment

“…The ability to synthesize tryptophan in the IFNg-rich infection microenvironment is an important virulence factor of the genital C. trachomatis serovars (Aiyar et al, 2014). IFN-g mediates the activation of host indoleamine 2,3-dioxgenase (IDO), leading to the consumption of tryptophan necessary for the growth of C. trachomatis and inhibiting the growth of C. trachomatis (Beatty et al, 1994;Aiyar et al, 2014;Olive and Sassetti, 2016;Molenaar et al, 2018). The tryptophan needed for the growth of C. trachomatis is reduced, and C. trachomatis forms a static state (Byrne et al, 1989).…”

“…After C. trachomatis escapes the host's immunity, the host's immune surveillance is reduced, and the environment is conducive to the growth of C. trachomatis, which is reactivated (Belland et al, 2003). After C. trachomatis reinfection or chronic infection, T helper (Th)1-, Th2-and Th17-type cells are triggered to mediate tissue destruction, fibrosis, and scarring, further leading to the progression of PID and its sequelae (Ziklo et al, 2016a;Molenaar et al, 2018).…”

The apparition macrophage and Döderlein bacillus is negatively correlated in class I Papanicolaou smear: A morphological examination

“…5 Döderlein's bacillus grow in the vagina possess the menstrual cycle and secrete acid, keeping the vagina acidic and repelling the growth of bacteria. [6][7][8] Postmenopausal women lose the environment in which Döderlein's bacillus grow due to reduced hormonal activity. Thus, it has been reported that the vaginal pH increases and the patient becomes susceptible to vaginitis.…”