*3.1. Endometriosis*

Dysbiosis in the GI tract disrupts immune function, which leads to the elevation of inflammatory cytokines and alteration of immune cell profiles. Those factors may play a role in the connection between the GI tract and endometriosis, as both have a high prevalence in patients [56]. As the GI tract possesses an organized lymphoid structure with many immune cells, the gut microbiota stimulates its growth and function, as shown in a study by Hooper et al. [57]. They further showed that dysbiosis alters the composition of immune cells, triggering inflammation [56]. In the case of the vaginal microbiota, it has been shown that a non-Lactobacillus-dominant (NLD) microbiota is associated with overgrowth of pathogenic bacteria, causing bacterial vaginosis. This may decrease reproductive potency, and a vaginal microbiota rich in *Gardnerella*, *Prevotella*, and *Bacteroides* sp. may increase the risk of endometriosis or pelvic inflammatory disease (PID) [58–62]. In recent years, it was also discovered that the uterus, previously thought to be a sterile environment, has its own microbiota. A healthy woman's microbiota consists primarily of *Firmicutes*, *Bacteroides*, *Proteobacteria*, and *Actinobacteria*, according to a study by Baker et al., and a review by Moreno et al. identified the five most represented genera in the endometrial microbiota [62–64].

Ata et al. studied women with stage III/IV endometriosis and compared their microbiota from the gut, cervix, and vagina to that of a control group of healthy women. The cervical microbiota of women with endometriosis had an increased number of pathogenic species, and stool samples had higher *Shigella* and *Escherichia* concentrations [65]. Other studies also found a correlation between the increase in bacteria associated with bacterial vaginosis or opportunistic pathogens in the reproductive tract with endometriosis in women [61,65–74].
