{"paper_id":"aa361bdd-b662-43de-8fd8-33e66f4da4a7","body_text":"REVIEW | OPEN ACCESS   \n \nMedical Science 29, e104ms3605 (2025)                                                                                                                                                                  1 of 8 \n \n Endometriosis and the \nMicrobiome: A Hidden Link in the \nFemale Reproductive Ecosystem \n \nSara Hassan1, Szymon Bienia2 ⃰, Aisha Hassan3, Kamil \nHassan4 \n \n \nABSTRACT \nEndometriosis involves the persistent presence of endometrial -like tissue growing \noutside the uterus. These lesions respond to hormones, break down, and cause \ninflammation. This disease mainly affects women of reproductive age and is often \naccompanied by unpleasant symptoms such as pain and infertility. To this day, the \nactual cause of endometriosis has not been identified. There are many theories, such \nas coelomic metaplasia or retrograde menstruation, but they do not offer a complete \npicture of the cause.  In recent years, research has emerged concerning the gut \nmicrobiome’s potential role as a contributing factor to the development of \nendometriosis. Results show that women with endometrial lesions exhibit a \nmodified gut microbial composition, with an overgrowth of harmful bacteria (such \nas Pseudomonas) and a reduction in those with more beneficial effects (such as \nRuminococcus). These changes may impact hormone metabolism and immune \nfunction, contributing to disease development. This has led to the “gut-reproductive \ntract axis” hypothesis — the idea that the digestive and reproductive systems \ninteract via immune and hormonal pathways. Microbial imbalances in one system \nmay trigger inflammation in the other.  Laparoscopy remains the gold standard for \ndiagnosis, but it’s invasive and often delayed due to overlapping symptoms. If \nmicrobial patterns are strongly linked to endometriosis, they could lead to non -\ninvasive diagnostic methods.  The gut microbiome is also being explored as a \ntherapeutic target. While human data are limited, probiotics might one day support \nstandard treatments. Large-scale clinical trials are needed to validate these findings. \n \nKeywords: endometriosis, gut microbiota, dysbiosis, probiotics, inflammation \n \n \n1. INTRODUCTION  \nEndometriosis is a chronic, estrogen -dependent condition characterized by the \npresence of functional endometrial -like tissue outside the uterine cavity. These \nectopic lesions, composed of both glands and stroma, exhibit cyclical activity in \nresponse to hormonal fluctuations, mirroring the behavior of the eutopic \nendometrium. However, in the absence of a physiological outflow pathway, this \nactivity results in localized inflammation, fibrosis, and the formation of adhesions, \nMedical Science \n \n \nTo Cite: \nHassan S, Bienia S, Hassan A, Hassan K. Endometriosis and the \nMicrobiome: A Hidden Link in the Female Reproductive Ecosystem. \nMedical Science 2025; 29: e104ms3605 \ndoi: https://doi.org/10.54905/disssi.v29i161.e104ms3605     \n \nAuthors’ Affiliation: \n1Medical University of Silesia, 18 Medyków Street, 40-752 Katowice, \nPoland; Email: sara.hassan2605@gmail.com; ORCID: 0009-0009-3297-\n8250 \n2Medical University of Silesia, 18 Medyków Street, 40-752 Katowice, \nPoland; Email: szymonbienia1@gmail.com; ORCID: 0009-0000-7632-\n5125 \n3Cardinal Stefan Wyszyński University in Warsaw, Wóycickiego 1/3, \n01-938 Warsaw, Poland; Email: 114039@student.uksw.edu.pl; ORCID: \n0009-0001-5078-7724 \n4Social Academy of Sciences in Łódź, Henryka Sienkiewicza 9, 90-113 \nŁódź, Poland; Email: hassimma99@gmail.com; ORCID: 0009-0008-\n3207-4836 \n \n⃰ Corresponding author \nSzymon Bienia \nMedical University of Silesia, 18 Medyków Street, 40-752 Katowice, \nPoland \nEmail: szymonbienia1@gmail.com \nORCID: 0009-0000-7632-5125 \n \nPeer-Review History \nReceived: 03 June 2025 \nReviewed & Revised: 07/June/2025 to 05/July/2025 \nAccepted: 07 July 2025 \nPublished: 12 July 2025 \n \nPeer-review Method \nExternal peer-review was done through double-blind method. \n \nMedical Science \npISSN 2321–7359; eISSN 2321–7367 \n \n \n© The Author(s) 2025. Open Access. This article is licensed under a Creative \nCommons Attribution License 4.0 (CC BY 4.0)., which permits use, sharing, \nadaptation, distribution and reproduction in any medium or format, as long \nas you give appropriate credit to the original author(s) and the source, \nprovide a link to the Creative Commons license, and indicate if changes were \nmade. To view a copy of this license, visit \nhttp://creativecommons.org/licenses/by/4.0/. \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \nDISCOVERY \nSCIENTIFIC SOCIETY \n \n\n \nREVIEW | OPEN ACCESS   \n \nMedical Science 29, e104ms3605 (2025)                                                                                                                                                                  2 of 8 \ncontributing to the hallmark symptoms of the disease: pelvic pain, dysmenorrhea, dyspareunia, abnormal uterine bleeding, and \ninfertility (Moïse et al., 2025). \nEpidemiological data suggest that endometriosis affects approximately 10% of women of reproductive age, with markedly higher \nprevalence among individuals experiencing reproductive disorders (20–50%) and those with chronic pelvic pain (up to 80%) (Parasar et \nal., 2017). Although most commonly diagnosed in women in the 20 -40 age group, the disease has also been documented in adolescents \nand postmenopausal women, underscoring its complex and multifactorial pathophysiology. \nThe exact etiology of endometriosis remains unknown to this day. Several mechanistic theories have been proposed, including \nretrograde menstruation, coelomic metaplasia, Müllerian remnant activation, and stem cell involvement (Lamceva et al., 2023).  More \nrecent hypotheses emphasize the role of uterine microtraumas and inflammatory processes at the endometrial -myometrial junction, \nwhich may facilitate the proliferation and ectopic implantation of endometrial cells (Zhai et al., 2020). Yet, none of these models fully \ncapture the heterogeneity of clinical presentation, disease progression, or patient response to treatment. These doubts regar ding the \ncorrectness of the diagnosis significantly prolong the time to diagnosis and treatment. \nOver the past decade, growing interest has emerged in the potential role of the human microbiome, particularly the gut microb iota, \nin the pathogenesis and symptomatology of endometriosis. The gut microbiome represents a complex and varied ecosystem made up  \nof trillions of microorganisms that collectively perform essential functions, including nutrient metabolism, immune regulatio n, \nepithelial barrier maintenance, and hormone modulation. Disruption of this balance, known as dysbiosis, has been implicated in a wide \nrange of inflammatory and autoimmune conditions (Zhang et al., 2025). \nAn additional, recently discovered fact, beyond the influence of the gastrointestinal tract, is a broader interaction between  the gut \nand the female reproductive tract, which has been termed the \"gut -reproductive tract axis.\" This theory sheds light on the two -way \ninteraction between the gastrointestinal and gynecological systems, driven by immune and hormonal factors. The close anatomic al \nrelationship between these systems, along with additional vascular and lymphatic connections, further supports the validity o f this \nhypothesis (Escorcia et al., 2025). \nMany women with endometriosis report gastrointestinal complaints that mimic irritable bowel syndrome (IBS), including bloatin g, \nconstipation, and altered bowel habits (Malin et al., 2015). These symptoms often lead to misdiagnosis or delayed recognition  of \nendometriosis. Searching for new biomarkers associated with changes in the microbiome may enable earlier and much less invasi ve \ndiagnosis of endometriosis compared to laparoscopy (Imperale et al., 2023). \nEarly-stage studies have shown notable differences in the microbial composition of stool, cervical mucus, and peritoneal fluid \nbetween women with endometriosis and healthy controls (Xholli et al., 2023). Reductions in anti -inflammatory genera such as \nLactobacillus and Ruminococcus, along with an increase in potentially pathogenic species like Pseudomonas and Escherichia col i, have \nbeen documented in affected patients (Ser et al., 2023). These findings, although preliminary, suggest a possible diagnostic role for \nmicrobial profiling and, in the future, a therapeutic one as well. \nIn animal models, specific probiotic strains —particularly Lactobacillus gasseri —have demonstrated immunomodulatory effects \ncapable of reducing lesion volume and enhancing NK cell activation (Itoh et al., 2011). Although clinical trials in humans re main scarce, \nsuch evidence raises the possibility of incorporating microbiota -directed therapies into individualized endometriosis management \nstrategies, complementing hormonal or surgical interventions. \nUnfortunately, the diagnostics of endometriosis are currently minimal due to its chronic and recurrent nature. Therefore, its  proper \ntreatment requires the discovery of its factual basis. One of the hypothesis assumes the key role of the microbiome and its i nfluence on \nimmunological and hormonal pathways, knowledge of which could enable effective and rapid diagnosis of endometriosis, as well as its \ntreatment. \nIn our review, we examined existing scientific papers related to the topic of endometriosis and its association with changes in the \nmicrobiome, specifically gut microbial dysbiosis and its systemic impact. As a result of analyzing the current state of knowl edge, we \naim to highlight the diagnostic potential of microbiota analysis, as well as potential treatment options primarily related to  changes in \nthe microbiota, which simultaneously influence the development of endometriosis. \n \n2. REVIEW METHODS \nThis review was conducted through a comprehensive and systematic search of peer -reviewed literature focused on the relationship \nbetween endometriosis and the microbiome, with particular emphasis on gut dysbiosis and its potential role in disease develop ment, \nprogression, and treatment. A search was conducted using open -access medical databases, including PubMed, with keywords such as \n\n \nREVIEW | OPEN ACCESS   \n \nMedical Science 29, e104ms3605 (2025)                                                                                                                                                                  3 of 8 \n\"endometriosis,” \"gut health,” and \"inflammation” to identify relevant studies published between January 2009 and May 2025. A rticles \nwere selected based on their direct connection to the topic, as determined by title and abstract screening. This review exami nes current \nevidence on the gut microbiome in endometriosis to inform clinical diagnosis and treatment. The goal of this review is to hig hlight the \ndiagnostic and therapeutic potential of microbiota -based approaches and to underscore the need for further research in this promising \nand rapidly evolving field. \n \n3. RESULTS AND DISCUSSION \n3.1. Concepts on the etiology of endometriosis \nOne of the frequently cited theories is based on the phenomenon of reverse flow of menstrual blood through the fallopian tube s, which \noccurs in the majority of women, potentially causing the transplantation of fragments of the uterine lining into the new envi ronment \n(Weber et al., 2023). An alternative theory, coelomic metaplasia, refers to the ability of cells to undergo metaplasia and fo rm \nendometrial-like tissue, including both glands and stroma (Lamceva et al., 2023). Another theory proposes that endometriosis can be \nactivated by excessive uterine peristalsis, which leads to micro -injuries between the endometrium and the myometrium, releasing pro -\ninflammatory mediators that induce the expression of aromatase. Locally released estrogen further stimulates endometrial proliferation \nand angiogenesis. During the healing process, stem cells are released that migrate to the abdominal cavity, where they contri bute to the \ndevelopment of endometriosis. They can also invade the myometrium, causing adenomyosis (Gruber et al., 2021). However, it can not \nbe stated with complete certainty that any of the known theories represents the actual mechanism underlying the development o f \nendometriosis, which hinders the identification of an effective therapeutic option. \n \n3.2. Current clinical strategies used to identify endometriosis \nThe current scientific consensus is that there are three main types of endometriosis, which can be distinguished by their loc alization, \nendometrial lesions, and pathological structure: superficial peritoneal endometriosis (SPE), ovarian endometrioma (OMA), and deep \ninfiltrating endometriosis (DIE). Regardless of location, all of them are associated with similar symptoms (Hsu et al., 2010) . In the \nmentioned cases, collecting a thorough medical history and a physical examination are the basis for a correct diagnosis and \nimplementing appropriate treatment. Besides symptoms suggesting a gynecological issue, patients might also show signs commonl y \nlinked to gastrointestinal or urinary tract disorders. For this reason, other possible causes must be ruled out before conclu ding that the \nsymptoms are due to endometriosis. Unfortunately, the detection of peritoneal endometriotic lesions still relies on laparosco py, as no \ncurrent imaging technique matches its sensitivity and specificity (Imperale et al., 2023). \n \n3.3. Microbiome-endometriosis correlation \nThe microbiome consists of all the microorganisms present in a given environment, such as bacteria, fungi, viruses, and archa ea. The \nhuman body harbors a microbiome that varies extensively by location, depending on factors such as pH, oxygenation, and the pr esence \nof particular nutrients (Blum, 2017). For instance, the gastric microbiome, being highly acidic, supports acid -tolerant genera such as \nPrevotella, Streptococcus, and Veillonella. The colon, however, being more neutral and anaerobic, harbors a more abundant and  \ndiverse microbial population, including species of the genus Lactobacillus, Akkermansia, and Enterobacter, among many others \n(Hollister et al., 2014). \nThe gut microbiota has a key function in several essential physiological activities. These involve breaking down and absorbin g \nnutrients, as well as vitamin production, the regulation of metabolic activity, the stimulation of angiogenesis, and the prom otion of \nrepair and regeneration of epithelial tissue (Ramakrishna, 2013). Besides these local effects, there is mounting evidence tha t the gut \nmicrobiome exerts a systemic influence, most prominently through its interaction with the immune system. Disruptions in micro bial \nbalance, or dysbiosis, have been linked to the development of various chronic diseases, including autoimmune diseases, metabo lic \nsyndrome, and inflammatory diseases (Durack et al., 2019). Much of this effect is thought to originate from the microbiota's capacity to \nregulate inflammatory signaling pathways and guide immune responses at both mucosal and systemic levels (Costello et al., 2015). \nThis is particularly relevant in the context of endometriosis, where immune dysregulation and chronic inflammation are firmly  \nestablished as central features of the disease pathology. Interestingly, heightened levels of pro -inflammatory cytokines have been \nuniversally demonstrated in the peritoneal fluid of women with endometriosis, indicating an aberrant immune response in the p elvic \nenvironment. Since gut microbes have been shown to affect cytokine production and immune cell function, it is not illogical t o \nimplicate dysbiosis in the initiation or perpetuation of inflammatory processes in endometriosis.  \n\n \nREVIEW | OPEN ACCESS   \n \nMedical Science 29, e104ms3605 (2025)                                                                                                                                                                  4 of 8 \nFurthermore, microbial flora of the lower genital tract, specifically the vaginal and cervical environments, has also been of  interest. \nThese communities are typically dominated by Lactobacillus species, which establish a stable, low -pH niche that confers protection \nagainst pathogenic organisms. Vaginal microbiota profiles are categorized based on the Community State Type (CST) model, and CST \ntypes I to III and V are considered healthy, predominantly dominated by Lactobacillus crispatus, gasseri, iners, and jensenii. In contrast, \nCST IV is associated with bacterial vaginosis and contains a higher proportion of anaerobic species such as Gardnerella, Atop obium, \nand Mobiluncus (Molina et al., 2022; Dong et al., 2024). \nThese microbiological changes are not constant and vary throughout a woman’s life, depending on hormonal disorders, sexual \nactivity, menstruation, and other behavioral or environmental factors. The dynamic nature of the microbiome suggests that it not only \nresponds to physiological changes but may also regulate disease risk. With immune -modulatory functions of numerous microbial \nspecies—some promoting inflammation, while others dampening it —ongoing research continues to investigate whether the \nmicrobiome plays an active role in endometriosis pathogenesis and development, or whether it simply mirrors an underlying dys biosis \nbrought about by the disease process itself. \n \n3.4. Probiotics as a supportive strategy in Endometriosis management \nAlthough clinical trials in humans are still limited, promising results have been obtained from preclinical studies in animal  models. \nOne of the best-known examples is a study published in 2011, in which mice with induced endometriosis were orally administered the \ninactivated L. gasseri OLL2809 for 21 days. (Itoh et al., 2011). The effects were compared with a control group and a group r eceiving \ninterleukin-12 (IL -12), known to activate NK cells. In the study, it was observed that the administration of L. gasseri OLL2809 \nsignificantly reduced the development of endometrial lesions, achieving an effect comparable to that of IL -12. Although no significant \nchanges were observed in peritoneal fluid cytokine levels or NK cell cytotoxicity, gene expression analysis revealed increase d \ntranscription of IL -2 and NCR1 genes in peritoneal cells, suggesting NK cell activation. Based on this study, the conclusion emerged \nthat L. gasseri may inhibit the development of endometrial lesions by acting as an immunomodulatory agent.  \n \n3.5. Available treatments for endometriosis \nUnfortunately, as of today, there is no way to cure endometriosis completely, but there are ways to alleviate the symptoms as sociated \nwith it, such as pain and infertility. There are various treatment methods available, including hormone therapy, pain medicat ions, and \nsurgery (table 1).  \n \n3.5.1. Hormonal therapy \nHormonal therapy is a standard approach in managing pain associated with endometriosis. Since endometriotic lesions respond t o \nhormonal fluctuations in a way similar to the endometrium, suppressing hormone production can reduce symptoms and lesion acti vity \n(Vannuccini et al., 2022). Hormonal treatment may help prevent the formation of new lesions and adhesions, but it will not di ssolve \nexisting adhesions. \n \n3.5.2. Pain medications \nAnalgesic effectiveness is based mainly on non -steroidal anti-inflammatory drugs. Since evidence of the efficacy of these medications \nfor relieving endometriosis -associated pain is limited, further research is needed on the use and effectiveness of different types of \nanalgesics in pain relief in endometriosis (Allen et al., 2009). \n \n3.5.3 Surgical treatments \nThe gold standard in surgical treatment of endometriosis is laparoscopy. It enables the assessment of the extent of endometrial changes, \nthe collection of a sample for histological and pathological examination, and the removal of endometrial foci. Possible inter ventions for \nendometriosis include diagnostic laparoscopy, excision and/or ablation of lesions, conscious pain -mapping laparoscopy, \nmicrolaparoscopy, and adhesiolysis (surgical removal of adhesions). In some cases, procedures targeting nerve pathways, such as \nuterosacral nerve ablation (UNA) or presacral neurectomy, may be performed to reduce chronic pelvic pain. Additional options \ninclude pelvic vein ligation (via surgery or interventional radiology), hysterectomy (total or subtotal), oophorectomy, and \nventrosuspension (Leonardi et al., 2021). \n\n \nREVIEW | OPEN ACCESS   \n \nMedical Science 29, e104ms3605 (2025)                                                                                                                                                                  5 of 8 \nPatients need a complete understanding of surgical treatment because the effects of some procedures are irreversible and may have \na significant impact on future fertility. This is why it is crucial for patients to discuss available treatment options with their healthcare \nteam before making definitive decisions. \n \nTable 1. Endometriosis Treatment Methods Overview \nTreatment Method Description Effectiveness/Limitations Key references \nHormonal therapy \nSuppresses hormone \nproduction to reduce \nendometriotic lesion \nactivity. Mimics \nendometrial suppression \nto manage pain. \nHelps reduce symptoms and \nprevent new lesions or adhesions; \ndoes not remove existing ones. \nVannuccini et al., 2022 \nPain Medication \n(NSAIDs) \nPrimarily uses non-\nsteroidal anti-\ninflammatory drugs to \nalleviate pelvic pain. \nLimited clinical evidence for long-\nterm effectiveness; further studies \nneeded to assess optimal pain \nmanagement. \nAllen et al., 2009 \n \nSurgical Treatments \nLaparoscopy is the gold \nstandard: allows for \ndirect visualization, \nbiopsy, and removal of \nlesions. \nProcedures include lesion excision, \nablation, microlaparoscopy, \nadhesiolysis, and pain-mapping \nsurgery. Can also involve more \ninvasive steps like hysterectomy or \nnerve pathway interventions. \nLeonardi et al., 2021 \nNerve-Targeting \nProcedures \nMay include uterosacral \nnerve ablation (UNA), \npresacral neurectomy. \nAim to reduce chronic pelvic pain; \nsome procedures are irreversible \nand may impact fertility. \nLeonardi et al., 2021 \n \n3.6. Can microbiota be a diagnostic marker? \nDue to the nonspecific symptoms of endometriosis, identification can take over a dozen years. The gold standard – laparoscopic \ndiagnosis – is an invasive procedure. There is growing speculation that examining the microbiome may facilitate the diagnosis of \nendometriosis. However, to develop non-invasive diagnostic tools based on the microbiome, it is essential to characterize the microbial \nprofiles typically observed in individuals with endometriosis and to distinguish them from those found in healthy individuals  \n(Iavarone et al., 2023). The study by Khan et al., (2010) presents the correlation between the significant increase in E. col i bacteria levels \nin the menstrual blood of women with ovarian endometriomas and superficial peritoneal lesions compared to women with ovarian \nendometriomas alone.  \nHuang et al., (2021) conducted a study of 41 women, 21 with endometriosis and 20 healthy volunteers as a control group. Sampl es \nwere collected from all participants at three sites: stool, cervical mucus, and peritoneal fluid. The study aimed to compare the \ncomposition of the microbiota between groups and different body locations. Research has identified notable variations in the \nmicrobiota of patients with endometriosis and healthy individuals, with the most pronounced changes observed in fecal and per itoneal \nfluid samples. \nAmong the bacterial genera identified as promising biomarkers were Pseudomonas in the peritoneal fluid and Ruminococcus in th e \ngut. As a result of advanced analyses, scientists created models based on key microbiota taxa. As of today, research results indicate that \ngut microbiota has a higher diagnostic value than cervical microbiota in the diagnosis of endometriosis (Huang et al., 2021). \n \n4. CONCLUSIONS \nThe relationship between the microbiota of the gastrointestinal system and the formation of endometrial lesions has been docu mented \nin numerous studies. Dysbiosis specific to endometriosis has been identified in both fecal and peritoneal fluid samples, with  \ndistinguishing features that accompany the illness. These include the expansion of some harmful bacterial taxa at the expense  of anti-\n\n \nREVIEW | OPEN ACCESS   \n \nMedical Science 29, e104ms3605 (2025)                                                                                                                                                                  6 of 8 \ninflammatory bacteria, which is quite protective. Evidence suggests that Ruminococcus from the gut and Pseudomonas from the \nperitoneal fluid may serve as potential antagonistic microbial markers that could assist the development of non -invasive diagnostic \nmethods for endometriosis in the future. The data suggest that changes in the microbiome may underlie, modulate, or sustain t he \npathophysiological processes in endometriotic lesions, particularly with regard to immunomodulatory factors and estrogen \ninteractions on metabolism and biological actions. \nThere is an emerging trend in the so-called gut reproductive tract axis, which prompts scientists to consider that some regions of the \nbody may have a potential means of communicating with each other. Considering anatomical proximity and shared borders of the \ngastrointestinal tract with the reproductive system, scientists believe that a state of dysbiosis in the bowel leacan lto an impairment in \nthe body’s immune balance and local environment. \nIn conclusion, the gut microbiome represents a positive perspective on understanding and treating endometriosis. Although fur ther \nwork is needed to translate laboratory findings into clinical applications, the integration of microbiome science into gyneco logical \nresearch holds great potential to improve diagnosis, guide treatment, and ultimately enhance quality of life for women living  with this \ncondition. \n \nAuthor’s Contributions \nConceptualization: Sara Hassan, Szymon Bienia \nMethodology: Szymon Bienia, Aisha Hassan \nFormal analysis: Sara Hassan \nResources, data curation: Kamil Hassan \nInvestigation: Sara Hassan, Szymon Bienia \nWriting – original draft: Sara Hassan, Szymon Bienia \nWriting – review & editing: Sara Hassan, Szymon Bienia \nAll authors have read and agreed with the final, published version of the manuscript. \n \nAcknowledgments \nNo acknowledgment.  \n \nInformed consent \nNot applicable. \n \nEthical approval \nNot applicable. \n \nFunding \nThis study has not received any external funding. \n \nConflict of interest \nThe authors declare that there is no conflict of interest. \n \nData and materials availability \nAll data associated with this study will be available based on the reasonable request to corresponding author. \n \nREFERENCES \n1. 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