Endometriosis is an inflammatory disorder. Caused by the proliferation of
endometrial tissue outside the uterine mucosa. Progression results from elaborate
interactions among hormonal, immunological, and environmental factors. Growing
evidence indicates that the gut and reproductive tract microbiota play a key role in
the pathogenesis of endometriosis. In patients with endometriosis, an increase in
potentially pathogenic taxa, including Escherichia, Gardnerella, and Streptococcus, is
observed. Dysbiosis leads to the translocation of bacterial endotoxins
(Lipopolysaccharide (LPS)), activation of the TLR4/NF-κB pathway, and increased
production of pro-inflammatory cytokines (IL-6, IL-8, TNF-α), which promote
angiogenesis and the proliferation of endometrial foci. Furthermore, disturbances in
the activity of the enzyme β-glucuronidase, part of the oestrobolome, increase the
pool of active oestrogens, playing a role in disease progression. Despite the growing
number of studies, further prospective studies involving larger populations are
needed to standardise diagnostic methods and confirm the therapeutic potential of
microbiome modulation in treating endometriosis.
Keywords: endometriosis, gut microbiota, reproductive tract microbiota,
estrabolome
