Far from remaining static during pregnancy, the vaginal microbiota evolves, and this change has been previously linked to the risk of preterm labor and preterm birth.
Despite this, the links between vaginal microbiota and preterm birth are far from clear: studies to date have been single-center, with contradictory findings, perhaps due to a lack of adjustments for confounding factors, such as the mothers’ ethnic background.

To get a clearer picture, a study ¹ study utilized data from the geographically and demographically diverse US birth cohorts in the ECHO (Environmental influences on Child Health Outcomes) program, which was designed to study the impact of prenatal and early neonatal exposures on child health. 

The researchers sought to use these cohorts to identify robust vaginal microbiota signatures during pregnancy which, when combined with maternal factors, could predict the risk of giving birth before 37 weeks of gestation.

Maternal factors associated to the risk of preterm birth

Of the 677 births analyzed, 12% (73) were preterm. The results show just how unequally women (mean age in study: 28 years) are affected by this risk.

• For example, 84% of preterm births involved women who identified as Black,
• and 85% were mothers with public health insurance only.

The risks of preterm labor and preterm birth thus appeared to be unevenly distributed according to maternal characteristics.

As regards the microbiota, women with a vaginal (Community state type (sidenote: Community state types Five types of vaginal community have been identified, four dominated by lactobacilli (Lactobacillus crispatus, L. gasseri, L. iners, and L. jensenii) and a fifth characterized by a low lactobacilli content. ) ) dominated by lactobacilli other than L. iners were less affected by preterm birth. They accounted for 6.8% of preterm births and 28.8% of full-term births.

These findings suggest that a vaginal microbiota rich in Lactobacillus may be associated with greater vaginal stability during pregnancy.

Bacteria at risk with predictive value

Risk assessments highlight an increased risk of preterm birth among women with diverse non-Lactobacillus-dominant vaginal communities, or vaginal communities dominated by L. iners, compared to women predominantly harboring L. crispatus , which is considered more stable. 

This holds true even after adjusting for ethnicity, maternal age, education level, or parity. 

The researchers subsequently tried to predict this risk by testing several models. The best model combined the taxa Gardnerella vaginalis (associated with bacterial vaginosis), Prevotella timonensis, and L. crispatus with maternal factors (age, ethnicity, etc.). It achieved an AUC (sidenote: AUC (Area Under the Curve) A measure of a model’s ability to correctly distinguish between two classes (for example, “diseased” vs “healthy,” “positive” vs “negative”). It represents the area under a curve that plots the true positive rate (sensitivity) on the y-axis against the false positive rate on the x-axis. If the AUC equals 1, the model performs perfectly; above 0.80 it is generally considered very good, and above 0.90, excellent; at 0.5, it performs no better than random chance.
  ) (area under the curve) of 0.77—a performance deemed satisfactory by the authors for a clinical prediction tool.

Your skin is not a simple barrier; it is a living ecosystem. Millions of microorganisms, including bacteria, fungi, and viruses, make up your skin microbiome. Together, they help regulate your immune defences, strengthen protection against infections, and maintain the balance of your cutaneous barrier (sidenote: Cutaneous barrier The protective outer layer of skin that keeps harmful agents out and moisture in. The microbiome is a key living component of this barrier, disrupting the microbes means weakening the defence itself and reducing protection against environmental stressors. ) .
When this community is disturbed, the consequences can include inflammatory skin conditions such as atopic dermatitis or increased vulnerability to skin diseases.

UV radiation: not just a surface problem

We know that ultraviolet (UV) radiation damages the skin, it accelerates ageing, causes sunburn, and raises the risk of skin cancer with chronic exposure. What is less well understood is what it does to the microbial community living on the skin surface.
Researchers ¹ at the Leibniz Research Institute for Environmental Medicine (Duesseldorf, Germany), set out to answer that question directly.
 

Disruption starts in as little as 30 minutes

In a controlled clinical trial, 30 healthy male volunteers were exposed to solar-simulated UVA and UVB radiation at three doses, 0.5, 0.7, and 1.0 minimal erythema dose (MED), on defined areas of the lower back.
Skin swabs were collected at:

• 30 minutes,
• 24 hours,
• and 4 days after exposure and compared to non-irradiated control sites.

The results were clear: measurable changes in the skin microbiome were already detectable at 30 minutes, even at the lowest sub-erythemal dose, a level of UV that does not cause visible redness or sunburn.
The extent of microbial disruption was dose-dependent: the higher the UV dose, the more pronounced the shifts. Partial recovery was observed at 24 hours, but certain changes persisted at 4 days after irradiation, suggesting that exposed skin may retain a delayed microbial signature.

What this means for your skin health

These findings matter because sub-erythemal UV doses are not exceptional, they represent ordinary, everyday sun exposure.
A short walk, time near a window, or an overcast day outdoors can all deliver these levels.
The study raises an important question about photoprotection: if sunscreen protects the skin from UV-induced cellular damage, could it also preserve the integrity of the skin microbiome and its immune protection?

Among some women with high exposure to sexually transmitted infections (STIs), menstrual management can become a health issue, but also a matter of economic survival.
A study ¹ conducted in Kenya highlights a little-documented phenomenon: the impact of menstrual poverty on the vaginal flora of sex workers.

When periods become an economic issue

In contexts of severe poverty, women do not have access to conventional menstrual products.
In Kenya, 42% of sex workers use makeshift solutions to continue seeing clients during their period. More than 9 out of 10 sex workers wipe the inside of their vagina with cloth, cotton or toilet paper between clients.

More fragile vaginal flora

In a large majority of these women, almost 2 out of 3, the vaginal microbiota is diverse, and therefore less protective compared with profiles in which lactobacilli dominate. It is associated with a higher risk of infections. Among the 407 women followed in this study:

• 24.7% had acquired HIV,
• 42.2% had bacterial vaginosis,
• and 21.9% had chlamydia, gonorrhea or trichomoniasis,
• only 20% had no infection.

In contrast, microbiota dominated largely by protective lactobacilli, especially Lactobacillus crispatus (CST-I), which were less common in these women, were associated with better vaginal health and fewer STIs or bacterial vaginosis.

The role of menstrual products

Monitoring these sex workers shows that use of unsuitable menstrual products seems to go hand in hand with changes in the vaginal microbiota, and even dysbiosis.
However, these results should be interpreted with caution: many factors are interconnected, including financial hardship, number of clients and working conditions, and the differences fade when these biases are taken into account.
Nevertheless, these trends are drawing researchers’ attention. Especially as certain pathogenic bacteria associated with bacterial vaginosis, such as Prevotella bivia or Mobiluncus curtisii, are more common among users of inadequate menstrual products.

Solutions still being explored

In response to these findings, researchers are exploring possible interventions. The idea is to improve access to suitable protection in order to improve vaginal health. Among the solutions being studied are flexible menstrual discs, which can be worn during sexual intercourse and used over the long term, for up to 10 years, which could reduce costs, limit certain risky practices and improve these women’s comfort and intimate hygiene.

After the genetic testing trend, a new wave of self-testing is emerging: gut microbiome tests.
The idea is simple: analyze the bacteria present in your intestines from a stool sample collected using a testing kit and sent by mail.

You directly receive a “gut health profile,” without having to see a doctor, to detect any potential dysbiosis. In other words, these bacteria are used as indicators thought to reflect the balance of the gut flora. 
A booming market driven both by recent scientific discoveries highlighting the links between the microbiota and various digestive and metabolic diseases, such as obesity or certain cancers, as well as mental health disorders, but also its essential role in immune system development—not to mention the misinformation spread on social media.
All in a climate of confusion between at-home self-tests and research on medical tests in clinical settings.

Unreliable results

Are these at-home tests reliable? A team of researchers ³ set out to check this by evaluating seven commercial services. To do this, they used a standardized stool sample—the kind laboratories typically use as a reference—and sent it three times to each company, using each complete kit according to the provided instructions, just as a consumer would before sending it to the lab.

The results should discourage you from investing in these tests! There are many flaws:

• analytical methods vary significantly from one company to another at every stage, from sample collection procedures to the computer-based analysis of results and the assessment of gut microbiota composition.
• results vary significantly from one company to another: only one bacterial genus (Streptococcus) was found by all companies. In some cases, the differences were comparable to the natural variations seen between individuals! Even more surprising, a same company sometimes obtained different results from the same sample sent three times for analysis.
• regarding result interpretation, each company uses its own benchmarks. The result: findings can vary from one provider to another—or even within a same company, which may deem a same profile “healthy” in one analysis and “unhealthy” in the next! This leads to contradictory recommendations, which are nonetheless presented as “personalized” in the report provided to consumers.

Call for caution and improvement

These discrepancies pose a serious problem, with the risk of delayed diagnosis for patients seeking answers, who might self-medicate based on misinformation, particularly when trying to better understand certain illnesses or a persistent intestinal disorder.

Furthermore, as consumer demand continues, the study’s authors are calling for several improvements to ensure that a simple test kit result is not treated as a medical diagnostic tool:

• improve analytical quality,
• exercise caution when interpreting results,
• and establish common guidelines for the entire sector (from testing companies to all potential partners involved).

The aim: to standardize practices and restore confidence among both users and health authorities.

Mental health disorders, cancer, obesity: human gut microbiota has been linked to numerous diseases since the early 2000s. Thanks to extensive media coverage, studies are encouraging consumers to “test” their gut health. A potentially lucrative market for sellers of self-test kits: consumers collect a stool sample at home, send it to the lab and receive the results directly.

7 self-tests under scrutiny

A team ² compared the performance of seven gut microbiome testing services by submitting three replicates of a standardized human stool sample to each, the kind laboratories typically use for calibration.

First observation: microbiome testing methods vary greatly between companies (collection procedures, sequencing, analysis), with no common standard. 

Second limitation: results vary significantly from one company to another.

• Of the seven companies tested, three detected the presence of Clostridioides difficile in the standardized sample, while the other four reported it as absent.
• Only one genus (Streptococcus) showed consistent results across all methods, while Roseburia showed the greatest discrepancy.
• In some cases, differences in results for a same sample exceeded the biological variations seen between individuals!
• Finally, the same company sometimes reported inconsistent results after analyzing the same standard sample three times. 

A final challenge: interpretation of results.
Because there is no universal definition of a healthy microbiota, each company uses its own reference values for several key bacteria. As a result, the findings vary from one company to another.
Worse still: within a same company, results can vary across replicates, sometimes leading to conflicting recommendations (with the microbiota deemed “healthy” or “unhealthy” depending on the replicate). These differences—both between and within companies—lead to inconsistent health interpretations and advice.

The authors’ recommendations

Recognizing the demand from patients seeking answers to their health issues, the authors recommend two main areas for improvement:

• Improve clinical validity by consistently citing the literature for each health interpretation to justify statements and recommendations, and distinguishing between simple correlations and true causal relationships.
• Strengthen analytical performance and transparency through quality control standards (reference materials, known microbial communities, minimum detection limits).

They also emphasize the need to develop common guidelines for the industry, drawing on best practices from other diagnostic fields, in order to harmonize practices and build confidence among users and regulatory authorities.

Your mouth is home to hundreds of bacterial species, a bustling invisible city that does far more than freshen breath. It shapes how your immune system reacts and, because the mouth opens straight into the airways, it shapes the lungs that sit just below. Chinese researchers ¹ wanted to know what happens to that city when ozone, the sharp, sunlit pollutant rising over our urban skies, drifts in.

A two-hour ozone, and everything shifts

Twenty-nine healthy young adults spent two hours inside a sealed chamber, breathing either filtered air or ozone at roughly the level of a bad summer smog day. Two weeks later, they switched. Nobody knew which air they were getting.
The difference was striking: after the ozone session, lung power dropped sharply, the volume of air the participants could forcefully exhale fell by around 12%, and the speed of that exhale by 14%.
That is not abstract. That is the feeling of climbing stairs and noticing, for the first time, that you are counting them.

The clue is in your mouth

Then the scientists swabbed cheeks and throats. Ozone had thinned the oral microbial community by more than a fifth, whole species, simply gone after a single exposure.
One bacterium, called Treponema medium, more than doubled its numbers and stood out as the clearest fingerprint of ozone damage. Its rise tracked closely with the drop in breathing capacity, suggesting the mouth is not just a bystander but a messenger, carrying signals of pollution downward into the lungs.

Why men felt it harder

Curiously, the men in the trial took the bigger hit. Their lung scores fell; the women's barely moved.
Their oral microbes reshuffled more dramatically too. The reasons are still being pieced together, but animal studies hint at sex-specific immune wiring that makes male airways more reactive to oxidising gases. However, as the female subgroup was smaller, these sex differences need confirmation.
The takeaway is not panic, it is perspective.
The air you cannot see is having conversations with the organisms you cannot feel, and those conversations are rewriting your breath.

Inside every woman's body, a small, mostly invisible community of bacteria lives in balance in the vagina. When it's dominated by lactobacilli, it guards against infection like a tightly packed hedge keeping weeds out.
Italian researchers wanted to know something new about that hedge: is it also quietly storing genetic instructions for resisting antibiotics, and if so, what in your daily life is feeding that archive?

A résumé written in your bacterial DNA

The team asked 105 healthy young women to self-collect their vaginal microbiome with swabs, none of them pregnant, none on antibiotics in the past month, and hunted for 14 different resistance genes.
The result was striking. Five of those genes, including ones that shield bacteria from two of our most-prescribed antibiotic families, erythromycin-type (like erm(F)) and tetracycline-type (like tet(M)), showed up in more than two-thirds of participants.
Most women were unknowingly walking around with a small dossier of instructions for shrugging off common antibiotics, tucked inside bacteria they had never thought about.

When more diversity means less health

Here the story flips what many of us assume. In the gut, a diverse microbiome usually means a healthy one. In the vagina, the opposite tends to be true: a thriving single bacterial species, Lactobacillus crispatus, is the sign of balance.

The researchers found that :

• the more crowded and mixed the vaginal community became, the more it drifted toward Gardnerella, Prevotella and other dysbiosis-linked bacteria, the more resistance genes accumulated.
• By contrast, L. crispatus was associated with fewer resistance genes, almost like a gatekeeper turning them away.

The everyday choices the genes respond to

What made the gene count climb? Smoking tripled the odds of carrying one specific resistance gene.
A higher body weight nudged the numbers up. A vaginal yeast infection was linked to almost four times the overall resistance score. Even unused antibiotics from the past year left a trace.
What seemed to push back? Oral contraceptives, a Mediterranean-style diet, and simply understanding how antibiotics work and why finishing the course matters.

Immune checkpoint inhibitors (sidenote: Immune checkpoint inhibitors (ICIs) Therapies that seek to remove the mechanisms that inhibit the immune system’s response to cancer cells. Targeted checkpoints include Programmed Death-1 (PD-1), Programmed Death-Ligand 1 (PDL-1), and cytotoxic T-lymphocyte associated protein 4 (CTLA-4). Lifting these brakes allows the immune system to recognize and attack cancer cells.
  ) (ICI) have improved the prognosis of non-small cell lung cancer (NSCLC) and cutaneous melanoma, but more than half of patients remain resistant.

Fecal microbiota transplant (FMT) could help overcome resistance to anti-PD-1 therapies (sidenote: Anti-PD-1 immunotherapy based on immune checkpoint inhibitors that target the PD-1 checkpoint, reversing the deactivation by the tumor of the recognition system associated with the PD-1 protein present on the surface of T lymphocytes. The immune system’s effectiveness against tumor cells is thus restored. ) : successful mouse trials, two Phase I clinical trials providing initial proof of concept, then the MIMIC Phase I trial demonstrating the safety of FMT from healthy donors to reduce primary resistance to anti-PD-1 treatment in patients with cutaneous melanoma.

Confirmed efficacy in Phase II

Hence the interest in the multicenter Phase II FMT-LUMINate trial, evaluating FMT from healthy donors combined with anti-PD-1 monotherapy in NSCLC (n = 20) or with dual immunotherapy (anti-PD-1 + anti-CTLA-4 (sidenote: Anti-CTLA-4 immune checkpoint inhibitor that targets the CTLA-4 checkpoint ) ) in cutaneous melanoma (n = 20). Eligible patients received one dose of FMT before immunotherapy. Ten healthy volunteer donors (10 in the NSCLC cohort, 6 in the melanoma cohort) provided stool samples.

The results demonstrate the clinical efficacy of FMT:

• for NSCLC, combined with anti-PD-1 therapy, the objective response rate (ORR) (sidenote: Objective response rate (ORR) Proportion of responding patients (who showed a complete or partial response), as opposed to patients with stable disease or disease progression. ) was 80% (16 of 20 patients), exceeding the predefined primary objective of 64%. Without FMT, ORR ranges from 39 to 45%.
• for melanoma, combined with anti-PD-1 and anti-CTLA-4, ORR was 75% (15/20) vs. 50–58% without FMT.

The disappearance of harmful bacteria

After FMT, patients’ gut microbiota was modified, without strong similarity to the donor. More importantly, the authors show that the clinical response is not related to the acquisition of new bacteria from the donor; it depends mainly on the disappearance of bacteria present in the patient before treatment, including species such as Enterocloster citroniae, E. lavalensis and Clostridium innocuum. Enterocloster and Clostridium spp. are known to be associated with poor response to immunotherapy and sometimes with unfavorable inflammatory profiles.

This loss of certain bacteria changes microbial metabolism, reducing tryptophan pathways involved in immunosuppression, and creates a more favorable immune environment with more cytotoxic T cells and fewer regulatory cells.

Safety assessment of FMT

In terms of safety, FMT was well tolerated in patients with NSCLC receiving anti-PD-1, with no adverse events of grade ≥3.

However, in the melanoma cohort receiving dual immunotherapy, adverse events were observed in 65% of patients, as well as a higher-than-expected rate of myocarditis in those who received FMT from a donor whose microbiota was enriched with Prevotella, including Segatella copri (sidenote: Segatella copri Segatella copri: formerly named Prevotella copri clade A., P. copri is not a single homogeneous species but a complex made up of 4 distinct genetic lineages (clades A, B, C, and D) with strong functional diversity. These lineages are often found together in non-Westernized populations (presence of all 4 clades, sometimes except D) but are much less frequent in Westernized populations (presence of A and B, A, or none). The decline of P. copri in Western-lifestyle populations may be linked to lifestyle and dietary changes associated with modernization. Source: Tett A, Huang KD, Asnicar F et al. The Prevotella copri Complex Comprises Four Distinct Clades Underrepresented in Westernized Populations. Cell Host Microbe. 2019 Nov 13;26(5):666-679.e7. ) . These adverse events were not seen in NSCLC patients treated with anti-PD-1 alone and receiving FMT from the same donor. This suggests an interaction between microbial taxa (involving Prevotella) and the type of immunotherapy (dual PD-1/CTLA-4).

Vitiligo affects up to one in fifty people worldwide. It appears as pale, depigmented patches where the skin's pigment-making cells, melanocytes (sidenote: Melanocyte The specialised cell that produces melanin, the pigment giving skin its colour and protecting it from sunlight. When melanocytes are damaged or destroyed, as in vitiligo, the skin loses its tone in the affected areas. ) , have fallen silent or died. For decades, dermatologists have focused on calming the skin itself, with steroid creams, ultraviolet lamps and, increasingly, lasers. Yet patches often return. A team of Chinese researchers ¹ suspected the real trouble might be starting somewhere else entirely: the gut.

A long-distance signal between gut and skin

Using a mouse model of vitiligo, the team showed that when they wiped out the animals' gut bacteria with antibiotics, the depigmenting patches shrank and the skin's level of oxidative stress (sidenote: Oxidative stress A chemical imbalance inside cells in which reactive, unstable molecules, often compared to sparks, begin to damage proteins, DNA and membranes. In vitiligo, this slow-burning damage is thought to push melanocytes toward death. ) , a kind of cellular rusting that damages melanocytes (sidenote: Melanocyte The specialised cell that produces melanin, the pigment giving skin its colour and protecting it from sunlight. When melanocytes are damaged or destroyed, as in vitiligo, the skin loses its tone in the affected areas. ) , dropped sharply. 

But when they placed different groups of vitiligo-affected mice together in the same cage, allowing their microbes to mix, the younger animals co-housed with older mice developed worse patches than those kept apart. The gut, it seems, was quietly pulling strings far above its own address.

Meet hippuric acid, the unlikely messenger

Screening hundreds of molecules in feces, blood and skin, the scientists kept arriving at the same suspect: hippuric acid (sidenote: Hippuric acid A small molecule made when gut bacteria digest plant compounds found in fruits, vegetables, tea and coffee. Normally harmless, it turns out to rise sharply in vitiligo and, this study argues, travels from gut to skin to fuel the damage there. ) , a small acid that gut microbes help produce from plant compounds in food. In vitiligo mice, hippuric acid was piled up in the skin at roughly five times normal levels. Injected into healthy mice, it reproduced the same chemical damage. Even more telling, when the researchers measured blood from 15 people with active vitiligo, their hippuric acid was nearly twice that of healthy volunteers.

A leaky barrier and a surprising treatment hint

How did a gut molecule reach the skin in such quantities? The vitiligo mice had fewer goblet cells, the tiny factories that line the intestine with protective mucus. With that inner lining thinned, hippuric acid slipped more easily into the bloodstream and travelled outward, ultimately latching onto two proteins in skin cells, NOS2 and MAPK14, that crank up oxidative damage.

The hopeful twist: feeding the mice a probiotic mixture visibly slowed their depigmentation. For a condition that carries a quiet emotional weight for millions, that is a new direction worth watching. Human trials will need to confirm it, but the finding opens a therapeutic door vitiligo has rarely looked through.

Allergic diseases (eczema, asthma, food allergies) often appear very early in life and are becoming more common. They therefore raise a crucial question: how do these allergic traits develop? And how can we counter them?

A question of bifidobacteria

A study ¹ published at the beginning of 2026 in the journal Nature Microbiology suggests that part of the story unfolds very early, through bacterial colonization of infants’ guts. In particular, certain bifidobacteria carry a specific gene (ALDH) that allows them to transform aromatic amino acids from breast milk into their respective aromatic lactates.

These lactates have a beneficial effect on the child’s developing immune system. One of them in particular is 4-OH-PLA, an aromatic lactate that appears to reduce the production of antibodies called IgE (immunoglobulin E), involved in the development of allergies. It is also associated with a lower incidence of atopic dermatitis at two years of age.

A very short time window

These processes occur early and pass quickly: the protective effect of ALDH+ bifidobacteria in the gut microbiota is thought to exist for only a very limited period, up to 5 to 6 months of age. During this period, which generally corresponds to breastfeeding, bifidobacteria are most abundant in the digestive system and 4-OH-PLA production is at its peak. The diversification of the diet (introduction of solid foods) then changes everything.
There may thus be a “critical window” in the infant’s immune development during which a gut microbiota rich in ALDH+ bifidobacteria can have a lasting influence on allergy risk later in childhood and adulthood.

Factors that support this protective mechanism

According to the study, several early factors seem to be linked to a better establishment of these beneficial bacteria and therefore to higher levels of 4-OH-PLA: 

• vaginal delivery, which allows the child to acquire part of the mother’s microbiota, including bifidobacteria;
• the presence of older siblings, also sources of joyful (and beneficial!) bacterial exchange;
• and, above all, exclusive breastfeeding during the first two months, which supports the development of natural protection mechanisms against allergies.