Gut microbiota composition in women with polycystic ovary syndrome

The gut microbiota is increasingly viewed as an invisible organ-like system that not only plays an important role in a woman’s wellbeing but also affects the pathophysiology of some disorders such as polycystic ovarian syndrome (PCOS). Knowing about microbial metabolite pathways may elucidate effective treatments.

A recent meta-analysis that included 948 women with PCOS from 14 studies explored the relationships between gut microbiota among women from different regions and with different testosterone levels. Key findings revealed distinct gut microbiota compositions in PCOS patients compared with their healthy counterparts, and significantly different gut microbiota between PCOS patients with higher testosterone levels and those with lower testosterone levels. Also, gut bacterial genera differed among PCOS patients from different regions; European patients had high Alistipes levels, whereas Chinese patients had high Blautia and Roseburia levels.

These findings support current evidence showing that PCOS patients have fewer different types of bacteria and a less balanced microbial community compared with healthy women. The data also confirm the abundance in PCOS patients of specific bacterial genera such as Escherichia/Shigella and Alistipes, which are associated with insulin resistance and inflammation. This study implies that the gut microbiome is linked to various metabolic and hormonal disturbances associated with PCOS, which is compatible with previous research. Importantly, it demonstrates differences in bacterial taxa between Chinese and European women with PCOS, which may assist with personalised treatment strategies. Further research to determine PCOS-associated bacteria strains may enhance anti-PCOS microbial therapies and studies in different geographical regions would promote the global treatment of PCOS.

To conclude, characterising gut microbiota in PCOS patients from different countries may enable gut microbiota to act as a biomarker to distinguish different subtypes of PCOS, and thereby improve the clinical diagnosis and treatment of PCOS.

The role of the vaginal microbiota in women’s health

The human body hosts trillions of microorganisms, collectively known as the microbiome, residing in various locations and coexisting in a complex symbiotic partnership. Importantly, the vaginal microbiota influences women’s reproductive and overall health. Understanding this ecosystem could revolutionise the prevention and treatment of these conditions.

This review highlights the links between dysbiosis of the vaginal microbiota and gynaecological disorders, as well as pregnancy-related complications. Specifically, reductions in lactobacilli and an increased vaginal microbiota diversity are associated with human papillomavirus (HPV) infection, the formation of cervical lesions, and cervical cancer. A loss of vaginal Lactobacillus dominance can create a proinflammatory environment that compromises successful embryonic implantation, leading to infertility. An imbalance in the vaginal microbiome can trigger inflammation leading to pregnancy complications. Having fewer Lactobacillus species in the vaginal microbiome increases the risks of premature rupture of membranes, preterm birth, miscarriage, and ectopic pregnancy. Vaginal dysbiosis may contribute to insulin resistance, a hallmark of gestational diabetes mellitus, and greater diversity in bacterial composition has been found in severe preeclampsia. Testing for Prevotella bivia colonisation during pregnancy may help to predict and mitigate against hypertensive disorders during pregnancy.

This review underscores the key relevance of the vaginal microbiome in women’s reproductive and overall health. The composition of this microbiome can impact everything from fertility and pregnancy outcomes to infection susceptibility. The article covers various aspects of vaginal microbiota, including its relationship with immune system function, inflammation, and pathogen defence, and thereby offers a broad, holistic understanding of its role with generalisable insights into women’s health at large. Enhanced knowledge around how the vaginal microbiome influences health presents an important advance for early disease detection and prevention, instead of treating infections or conditions after they appear. However, long-term study data are needed to clarify the long-term effects of vaginal microbiome imbalances. Moreover, while probiotics and other microbiomebased interventions show promise for maintaining a healthy vaginal microbiome, probiotic strains, dosages, and delivery mechanisms have yet to be standardised for clinical application. Much work remains to be done.

In sum, having fewer vaginal Lactobacillus species and increased vaginal microbial diversity is associated with obstetric and gynaecological complications. This review highlights the possibility of using microbiome-based diagnostics to detect imbalances in vaginal flora, potentially before symptoms manifest. Early intervention may prevent adverse consequences.

Talk about vaginal infections, fertility, or pregnancy complications often focuses solely on women. But there is another important player: the male urogenital tact (MUGT). The wide variety of microbes in the MUGT can significantly affect female reproductive and vaginal health (Figure 1). Understanding these influences may improve outcomes for women, especially those with persistent vaginal infections, fertility challenges, and pregnancy complications.

Figure 1. Consequences of exchanges of bacteria associated with vaginosis during sexual contact between males and female

What do we know about the male genital microbiota?

The MUGT includes several distinct microbial environments: the skin of the penis, the urethra, semen, and the urinary tract. Each has a unique bacterial community, influenced by factors like circumcision, sexual practices, hygiene, and lifestyle.

MUGT microbiota vary with circumcision status, sexual practices, and the composition of the female partner’s vaginal microbiota⁷.
Interestingly, the urethral microbiota of homosexual men does not seem to be modified by the type of sexual intercourse (oral or anal)⁸. Bacterial exchanges between partners during sexual contact are the rule; why these exchanges lead to vaginal dysbiosis in some cases and not others is unclear.

Seminal microbiota are also influenced by several physiological functions (age, hormonal changes) and lifestyle or epigenetic factors
(tobacco, alcohol, obesity, high-fat diet, exposure to toxins)⁵. These modifiable factors are potential targets for intervention.

How does the MUGT impact female health?

The transmission of microorganisms responsible for bacterial and viral sexually transmitted infections (STIs) including HIV and herpes simplex virus infection during sexual contact is the most obvious consequence of how the MUGT impacts female health. The female complications of bacterial STIs (gonorrhoea, infections by Chlamydia trachomatis or M. genitalium) are well known (inflammation and infection of the upper genital tract, risk of tubal infertility).

Many studies have shown that the epidemiological profile of women with BV is comparable to that of women with STIs, suggesting possible sexual transmission of the bacteria involved in BV. The presence of BV-associated bacteria in the foreskin and urethra of partners of women with BV and a concordance of vaginal and male urethral bacterial strains support the sharing of these strains or sexual transmission of BV.

Treating the male partner with oral antibiotics (metronidazole) has had very limited impact on recurrence rates in women with recurrent
BV, although combining metronidazole with a topical antibiotic applied to penile skin in partners of women with BV may reduce the risk of recurrence⁹.

The impact of the MUGT on uterovaginal health is not limited to passive bacterial transfer. Seminal fluid contains proinflammatory substances (such as prostaglandins) that can interfere with immune responses and inflammation within the female genital tract¹⁰.

Founded in France in 2021 by the ENDOmind Association under the aegis of the Foundation for Medical Research, the Foundation for Endometriosis Research aims to accelerate research on a disease that affects one in 10 women: endometriosis. Each year, the Foundation funds research projects aimed at understanding the pathology of endometriosis, improving diagnosis and developing more effective treatments.

In 2024, the Foundation for Endometriosis Research Executive Committee decided to more clearly define its research priorities for endometriosis and maximise its research impact. To this aim, the Foundation coconstructed and co-funded an innovative collaboration with the Curie Institute in Paris, seeking to compare the cellular microenvironments of endometriosis lesions and ovarian cancer. This ambitious project is starting in 2025 and illustrates the Foundation’s desire to encourage cross-disciplinary and innovative research
approaches.

Furthermore, the Foundation for Endometriosis Research has initiated a multidisciplinary scientific investigation with European experts on the links between microbiota and endometriosis. The Foundation will call for expressions of interest later in 2025, with the objective of launching new research work at the start of 2026, with financial support.

By focusing its efforts on strategic themes, the Foundation for Endometriosis Research confirms its role in accelerating research and ultimately contributing to improving the quality of life for the millions of women affected by this still little-known disease.

Key achievements of the Foundation for Endometriosis Research:

What is the prevalence of endometriosis?

A.H.: Endometriosis is surprisingly common – as common as asthma and diabetes. It affects an estimated 1 in 10 women.

W.F.: In my practice of irritable bowel syndrome (IBS), it’s even more common – certainly more than 25%.

What are the signs and questions to ask to avoid missing a diagnosis?

A.H.: Signs are varied and diagnosis can be difficult. The main symptom is chronic pelvic pain, which can often be debilitating, disrupting life and work. But, patients can also present with painful sex, chronic fatigue, diarrhoea and/or constipation and urinary symptoms. Any cyclical symptom can be a red flag for endometriosis.

W.F.: Increased peristalsis and softer stools during menstruation are normal, but significant and cyclical diarrhoea may not be so. Pain is expected, but not to the point of being bedridden.

A.H.: Another symptom that causes alarm is infertility. But I reassure patients with endometriosis: two-thirds of them won’t have trouble getting pregnant, and those who do generally respond well to surgery or IVF.

W.F.: I would add that endometriosis is chronic, but that doesn’t mean it’s untreatable. It’s important that any specialist involved with the care of these patients reinforces that message.

How common are digestive symptoms in women with endometriosis?

A.H.: The true prevalence isn’t known, but nearly all my patients have digestive symptoms – bloating, bowel changes, heartburn. Lesions on the bowel wall explain some symptoms, but many have superficial peritoneal disease, making the link harder to define.

W.F.: I have observed similarly, and would state that inflammatory bowel disease (IBD) is four times more common in women with endometriosis compared with the general population (4% vs 1%). IBD and endometriosis are both autoimmune conditions; having one increases the risk of the other.

Is there a need for multidisciplinary management?

A.H.: Endometriosis is a systemic inflammatory disorder. As gynaecologists, we’re not equipped to manage digestive symptoms. In Edinburgh, I’ve recently set up a joint gynaecology–gastroenterology clinic.

W.F.: When the abdominal pain strictly relates to menstruation, the gastroenterologist may find it difficult to add much. When the relationship is more loosely defined, we should investigate. Persistent digestive symptoms despite treatment may signal coexisting IBS. Also, be mindful of medications, particularly nonsteroidal anti-inflammatory drugs (NSAIDs). Occasional use is fine in young patients, but chronic use may require a proton pump inhibitor (PPI), which can cause dysbiosis. There’s no universal rule — we must tailor care to each patient.

Are gut and vaginal microbiota involved?

A.H.: There’s growing interest in the role of the gut and vaginal microbiomes in endometriosis. Some studies suggest associations, but they’re small and flawed. We need large cohort studies. I believe the microbiome plays a role, but it’s still unclear as to which comes first — microbiome changes or endometriosis. If microbiota drive symptoms, this could open the path to new treatments.

W.F.: It’s an exciting field. In patients with endometriosis, we observe gut dysbiosis with reduced short-chain fatty acids like acetate, propionate and butyrate that protect gut permeability. The same pattern can be seen in other gastroenterological conditions, like IBS or IBD, but we don’t yet understand the relationship. Maybe one day, we’ll personalise care by restoring exact missing strains. For now, we don’t know what causes what, so mechanistic studies are needed.

Should we recommend specific diets to patients with endometriosis?

W.F.: There’s no universal diet for endometriosis and we shouldn’t offer false hope. Allergies, lactose intolerance, and coeliac disease might be involved. The best step is to refer patients to a nutritionist.

A.H.: No specific “endometriosis diet” exists, but many patients report symptom relief after dietary changes. In my clinic, patients work with a dietitian to carefully adjust their diets. In our international survey of 2,500 patients with endometriosis, some found relief by stopping consumption of alcohol and caffeine, or foods containing gluten. However, without guidance, dietary restriction can be harmful.

Historical perspective

The beginning of the long journey towards the understanding of the vaginal microbiome can be attributed to Albert Döderlein, at the end of the 19th century. In his book Das Scheidensekret und seine Bedeutung für das Puerperalfieberhe pointed out that “normal”, healthy women have the vagina dominated by Grampositive bacilli, which he named Lactobacillus acidophilus.

This concept still shapes contemporary interpretations of the vaginal microbiome, but the reality is probably far more complex.

Understanding of vaginitis is still incomplete, and its management mostly empirical, despite being one of the most common causes for  women to seek a medical appointment¹.

In 2011, Ravel et al. published one of the most important and mind-changing papers in terms of understanding of the human vaginal  microbiome. In that paper they demonstrated that asymptomatic is not synonymous with “normal” (leading also to the question of what 
is a “normal” – or, probably more accurate, “optimal” – vaginal microbiome) and that there are striking differences according to ethnicity².

Diversity is the rule in nature, but the human vagina seems to be an exception: the accepted “optimal” vaginal microbiome is dominated by one or two species of lactobacilli (low alpha diversity). If we think about other organs or anatomical regions, dominance by one species 
is usually synonymous with disease (infection). If we perform the same exercise considering any ecological system, it represents the last 
step before collapse (e.g. monocultures of plants never occur in nature, and when performed artificially they must be limited in time). We can look for further explanations for this apparent “abnormality” (or “exception”) in nature, but it does seem to lead to a dead end. 

Should we, instead, change the focus of our lens and investigate gene pools rather than species or genera to overcome this apparent 
biological abnormality

The ultimate goal of living beings seems to be passing genes to the next generations and evolution seems to be much driven by this 
primordial “instinct”. Therefore, we can easily assume that the human vaginal microbiome should be a fulcral part of the end-product 
of evolution to optimise the reproductive process. If this premise is correct, we can expect

1. evolutionary congruence (as has been shown, for instance, in the gut);
2. any differences should be more or less easily explained (mating process, diet, geographical location, etc.) and, naturally
3. higher similarity in closely related species.

Surprisingly, none of the three premises are satisfied. In nature, phylogeny cannot be related with the vaginal pH (a very indirect marker of the vaginal microbiome composition), and dominance by lactobacilli is unique to the human species. Even when comparing humans with other primates, the differences are huge and, currently, not easily explainable^3,4. What made the human vagina so unique? Was it the fruit of random events or the evolutionary corollary of the continuous ovarian cycle, high risk of lacerations and infection at birth, or agriculture and the consequent high consumption of starch³?

The microbiome and pregnancy

One issue seems to be beyond doubt: lactobacilli are fundamental for the success of pregnancy – but it is not so clear if the same 
applies to achieving a pregnancy⁵.

The available data clearly show that a vagina not dominated by lactobacilli during pregnancy is associated with negative obstetrical and puerperal outcomes, including preterm labour, premature rupture of membranes, and puerperal infections (Figure 1). Of note, one million babies die every year from prematurity-related complications⁶.

We are used to repeating that lactobacilli have a protective role and that their presence is desirable, but to assume that means we must ignore some obvious facts, such as that this dominance does not occur in children, during breastfeeding, nor in postmenopausal women. Therefore, we can theorise that our symbiotic relation with lactobacilli serves us a purpose during the reproductive years. We can consider that this purpose includes a reduction in the risk of sexually transmitted infection (STIs) (which pose a risk to the success of reproduction and to the offspring), of ascending genital infections (and consequent abortion, stillbirth, and preterm birth), as well as of puerperal complications. The role of the microbiome in achieving pregnancy seems to be more limited. For instance, populations with high rates of vaginal dysbiosis do not seem to be less fertile⁷

Figure 1. Vaginal lactobacilli dominance is associated with beneficial obstetrical and puerperal outcomes

In the same way, the impact of the cervicovaginal microbiome on the outcome of fertility treatments is also unclear⁵.

One of the biggest evolutionary differences between humans and other mammals has to do with delivery – the difficult balance between being born with a large cephalic perimeter and negotiating it with a pelvis that had to adapt to bipedalism. Humans have the most difficult deliveries – perhaps surpassed only by hyenas. Can this hold the key to understanding the uniqueness of the human vaginal microbiome? Whatever the evolutionary purpose was, for most women of reproductive age, even out of pregnancy, the dominance of lactobacilli in the vagina is the desirable state. But lacking lactobacilli, despite representing a dysbiotic state, is not synonymous with disease.

Our understanding of the role of the vaginal microbiota is still very limited. Even apparently simple questions, such as how lactobacilli
colonise the vagina still does not have a clear answer.

The vulvovaginal microbiome in heath and disease

The most noticeable effect of an altered microbiome is vaginitis. Most women will suffer at least one episode of candidiasis and, in some populations, more than half of reproductive-aged women have bacterial vaginosis (BV), asymptomatic most of the time (figure 2A and 2B). We have a limited understanding of what drives these shifts (“normal” – colonisation/asymptomatic state – symptomatic)⁸.

Figure 2. Microphotographs of wet mount microscopy preparations (phase contrast 400x)

(A) Normal lactobacilli, presence of Candida spp. blastospores (circle); (B) Bacterial vaginosis
(absence of lactobacilli and overgrowth of anaerobic and facultative bacteria).

However, the bacterial profile of the vagina,regardless of symptoms, may confer differentprofiles of risk or protection. In general, it is considered that Lactobacillus spp. tendto confer health benefits. However, not all species are equal and only a limited number of the existing species are usually found in dominating states in the vagina. L. iners, with a significantly smaller genome and different metabolic profile, is usually associated with dysbiotic or transition states⁹.

Table 1. Gynaecological and obstetrical conditions and their associations with the vulvovaginal microbiome.

While there are no current recommendations to treat asymptomatic dysbiosis (e.g. BV), it has been associated with obstetrical and non-obstetrical complications (including risk of acquiring STIs [HPV, HIV])⁸ (Table 1).

Once efficacious (preferably non-antibiotic) strategies are available, it may be advisable to screen and treat dysbiosis in women at increased risk of STIs or even in those infected with HPV. This, however, may prove more complex than it appears. The STI-like behaviour of BV has long been acknowledged, but recent data have confirmed it, as well as suggesting that reduction of recurrences may require treatment of partners, which may represent a great obstacle to prevention strategies¹⁰.

BV is a common syndrome, in which there is depletion of lactobacilli and an overgrowth of several strictly and facultative anaerobic bacteria, associated with formation of a biofilm that seems to contribute to the frequent relapses after treatment. The composition of BV is variable from woman to woman – and probably even in the same woman over time¹¹. Currently it is possible to diagnose BV using molecular tests, but it is expected that with the increasing knowledge of the vaginal microbiome, these tests will allow for the “profiling” of BV, the evaluation of the resistome, and a more rationale choice of treatments⁸.

The relationship between Candida spp. and the vaginal microbiome is very complex and far from fully understood. While candidiasis can exist with any vaginal microbiome, it tends to be more common with lactobacilli dominance (and the consequent low pH)¹².

Several gynaecological conditions have been associated with specific microbiome characteristics and, almost systematically, a reduction in lactobacilli confers an increased risk for STIs and gynaecological cancers (even of the upper genital tract). However, a causal relationship between the microbiome deviations and the specific conditions is not always straightforward. We can, however, expect to one day assess or modulate the risk of cancer through the evaluation of the vaginal microbiome – especially for cervical cancer¹³.

The interest and knowledge in the vulvar microbiome is more recent and the amount of data is scarce, but its role in entities such as vulvodynia, vulvar dermatoses, vulvar intraepithelial neoplasia and cancer is being studied^14-16.

What’s next?

Giant strides are being made towards the understanding of the vulvovaginal microbiome. Until we fully understand the microbiome, we can start by respecting it and its functional role, recognising that each woman is unique (and that this uniqueness is mutable), avoiding
unnecessary use of antibiotics and antiseptics, and properly diagnosing STIs and vaginitis, rather than relying on empiricism. Accurate diagnosis will minimise wrong treatments, with a potential long-term impact.

At this stage, it is essential to distinguish what is investigational and what is clinically relevant. We are in a process of learning and attempting to use investigational techniques and concepts in clinical practice that often leads to unnecessary testing, expenses, and
treatments – for instance, metagenomics is a very useful research tool, but it currently has no place in the clinical evaluation of vaginitis.

In the last two decades we have amassed a huge quantity of information, which will soon translate into better health care for women, including specific dietary recommendations, and pre- and probiotics. We can expect that this knowledge will substantially reduce preterm labour, gynaecological cancers, as well as the recurrence of vaginitis and cystitis.

The next chapters will undoubtedly be the most exciting ones!

A woman’s vaginal microbiota undergoes changes over the course of her life, sometimes to the point of shifting type, as shown by a study ¹ including 125 sexually active women aged 18 to 25 in the south of France (Montpellier).

Lactobacilli, guarantors of stability

The study’s first finding was that bacterial communities dominated by lactobacilli — rod-shaped bacteria known to be most beneficial to women’s intimate health — are more stable over time. In other words, vaginal microbiota rich in lactobacilli such as L. crispatus, L. gasseri, L. jensenii, or L. iners are more difficult to disrupt.

A balanced vaginal microbiota dominated by these lactobacilli will limit the proliferation of pathogens, but if too much stress is put on the microbiota, pathogens can proliferate anyway.

Drinking parties, disrupted vaginal flora

The second finding was the list of factors that can wreak havoc on our vaginal flora.

In the 125 students studied, alcohol was identified as the factor with the strongest and most consistent effect, promoting suboptimal flora and increasing vagina’s vulnerability to infections, particularly by facilitating proliferation of pathogenic bacteria.

Partners, hygiene, and antibiotics

Other factors may also influence the transition from one vaginal bacterial community to another:

• A higher number of sexual partners may increase the risk of maintaining (or switching to) non-optimal flora, thereby promoting the development of vaginal infections that can progress to bacterial vaginosis. 
   

• The effects of intimate hygiene products (creams, tablets, capsules, gels, and wipes) on women’s health appear to vary from one woman to the next, with possible circular changes from one type of flora to another. 

• As for antibiotic use — whether local treatments for bacterial vaginosis (genital application of metronidazole) or systemic treatments (oral antibiotics) — it appeared to be only loosely associated with transition to a different type of vaginal flora. This absence of an effect surprised the researchers: were the samples taken too far apart to “capture” any short-lived change in flora linked to antibiotics?

In zebrafish (Danio rerio), a bacterial protein promotes the proliferation of β cells in the islets of Langerhans. But what about mammals? Β-cells are necessary for sufficient insulin production, and their proliferation increases rapidly after birth, at the same time as the gut microbiota diversifies.

Is this a mere coincidence or is there a genuine correlation, as in zebrafish? A British team ¹ has settled the question by showing in mouse pups that postnatal β-cell development is stimulated by bacterial and fungal species during short colonization windows, periods also critical for metabolic health.

In mice and humans

By eliminating and restoring microbiota at different pre- and postnatal periods in mouse pups, the team identified a critical period (from 10 to 20 days after birth) during which the gastrointestinal flora is essential for the establishment of a normal mass of β cells. These observations were confirmed by experiments with antibiotics and antifungals, highlighting the involvement of bacteria and fungi in maintaining glycemic balance.

And in humans? Fecal samples from human infants aged 7 to 12 months (but not from other age groups) strongly stimulated β-cell mass in mice. Humans therefore also appear to have a window of colonization by microorganisms that promote β-cells.

This is yet another argument in support of the much-publicized 1,000-day window of opportunity for future health and the prevention of metabolic diseases such as obesity.

Bacteria and fungi responsible

The comparison of microbial communities capable of inducing (or not) β-cell development has identified bacterial and fungal taxa involved in the case of mice: Escherichia coli, Enterococcus gallinarum, and Candida dubliniensis. The latter proved to be the most effective, thanks to a mechanism involving macrophages and β-cells, which allows the recognition of specific signals from the cell wall of commensal yeasts.

Lastly, not only does C. dubliniensis reduce the prevalence and severity of diabetes in mouse models, but it also helps restore the β-cell population after ablation or underdevelopment following antibiotic treatment. By disrupting gut microbiota during early childhood, these treatments can alter glycemic regulation and interfere with the maintenance of stable body weight. Could C. dubliniensis be used prophylactically to make up for losses induced by antibiotic treatment, particularly in individuals predisposed to type 1 or type 2 diabetes or obesity?

Preventing or even reversing β cell loss?

This study shows that there may be a critical window in young children, between 7 and 12 months, during which certain bacteria and fungi are necessary for the development of β-cells in the pancreas. If this developmental window is missed, β-cell development may be compromised, leading to dysfunction and an increased risk of metabolic diseases such as obesity and diabetes.

However, the mechanisms identified by the authors of the study have the potential to prevent or even reverse the loss of β-cells, provided intervention comes early and takes into account the key role of the gut microbiota.

According to a new study, in women scheduled for endometrial polyp removal, a vaginal microbiota is well balanced before removing uterine polyps? According to a study published in the European Journal of Obstetrics and Gynecology, this may be the case. The authors, researchers at Nanning University in China, demonstrated that the presence of a vaginal dysbiosis was a major risk factor for the recurrence of polyps after surgical removal. ¹

The link between dysbiosis and recurrence results from the impact of this microbial imbalance on the vagina and uterus, two anatomical areas closely connected in terms of immunity and microecology.

Nearly 700 women enrolled

To obtain this result, the researchers collected vaginal secretion samples from 679 women aged 25 to 50 who were undergoing “hysteroscopic resection,” a procedure to remove endometrial polyps. 

After the procedure, the women were followed for two years and the researchers identified a recurrence of polyps in 105 of them.

An analysis of the secretions indicated that women who had vaginal dysbiosis before the operation were 3.3 times more likely to experience a recurrence. This was also the case for women with endometriosis.

An analysis of the microbiotes vaginauxindicated that, in women who suffered from recurrence, the density and diversity of bacteria, as well as the presence of Lactobacilli, were significantly lower than in those with no recurrence. There were also more pathogenic microorganisms, such as the bacterium Gardnerella vaginalis and the fungus Candida, which cause vaginosis and yeast infections, respectively.

The researchers also observed increased activity of certain enzymes, such as leukocyte esterase, a sign of persistent inflammation in the vagina, which can promote infection spreading upward to the uterus.

Decline in Lactobacillus, a key factor in recurrence

How are these abnormalities in the vaginal microbiota involved in the recurrence of polyps? The researchers believe the answer lies with Lactobacillus.

Under normal circumstances, these bacteria produce bacteriocins, substances capable of destroying pathogens, as well as lactic acid, which acidifies the vaginal environment and stabilizes microbiota. They also synthesize molecules called glycerophospholipids, which in turn promote secretion by the body of anti-inflammatory messengers called prostaglandins. Lastly, they increase the synthesis of proteins that are involved in the integrity of the vaginal wall.

Thus, by reducing the risk of infection and inflammation after surgery, Lactobacillus may help protect against polyp recurrence.

This beneficial action is all the more important in women with a history of chronic microbial imbalances or endometriosis, for whom the risk of recurrence is significantly higher.

Towards preventive treatments

The researchers highlight the importance of maintaining the balance of the vaginal microbiota, particularly the long-term dominance of Lactobacillus, in cases of uterine polyps. They suggest several possible preventive treatments:

• a combination of probiotiques and antimicrobials, which would make it possible to tackle immediate pathogenic imbalances while promoting long-term microbial health;
• lactic acid-based gels or vaginal suppositories;
• bacteriophages, viruses capable of selectively destroying pathogenic bacteria without disrupting the microbiota;
• prebiotics and omega-3 fatty acids, which promote balanced microbiota.

These modulation strategies could also improve overall vaginal health by reducing the risk of persistent infection.

While studies are still needed to evaluate the effectiveness of these interventions, these avenues are promising. Keep informed!