More than one in ten children worldwide are born prematurely (sidenote: Preterm birth birth before 37 completed weeks of gestation. There are sub-categories of preterm birth, based on gestational age:
- extremely preterm (less than 28 weeks);
- very preterm (between 28 and 32 weeks);
- moderate to late preterm (between 32 and 37 weeks). Source: WHO ) . A British team recently analyzed data from thousands of young mothers ¹ to show that blood type influences the composition of the maternal vaginal microbiota, and with it, immunity and pregnancy outcomes: women with blood type A may be better protected against certain infectious risks thanks to the increased presence in the vagina of beneficial bacterium, Lactobacillus crispatus.

How is this possible?

You’re probably aware that the four main blood types are A, B, AB, and O. These letters indicate the presence of large sugar molecules called antigens, of type A and/or B (or their absence in the case of type O), on the surface of red blood cells. Among other things, these groups determine compatibility for transfusions.

What is less well known is that these “marker” antigens are not only found in the blood: they are also present in other cells (e.g., in the vagina or cervix) and in bodily fluids (including those produced by the cervix and vagina). By contributing to the adhesion or feeding of bacteria, these antigens influence susceptibility to infections. For example, people with type O blood are statistically more vulnerable to Helicobacter pylori, while those with type B blood are more vulnerable to bacteria such as E. coli.

Does each blood type have its own vaginal flora?

Researchers have now confirmed that A, B, and O antigens play a role in vaginal microbiota composition. Women with blood type A are more likely to have a vaginal microbiota dominated by L. crispatus, a beneficial bacterium that very easily attaches to the A marker. A direct consequence of this connection is a less inflammatory vaginal flora and a higher chance of full-term delivery. 

Conversely, L. crispatus is often depleted in women with blood type O, particularly high-risk women due to a previous preterm delivery, and those with blood type B, who generally harbor more of the pathogen S. agalactiae, a bacterium that easily attaches to the B marker.

Not so fast

However, do not over-interpret these results, or take liberties with your vaginal flora if you’re in group A. The effect of blood type on the risk of preterm birth remains low and is much less important than factors such as ethnicity (African and Asian women are at higher risk) or medical history. This discovery should primarily be seen as a gateway to future antigen-based therapies aimed at preventing preterm births.

Neoadjuvant immunochemotherapy is seen as a major advance in the treatment of esophageal squamous cell carcinoma (ESCC) (sidenote: Esophageal Squamous Cell Carcinoma (ESCC) Type of esophageal carcinoma (EC) that can affect any part of the esophagus, but is usually located in the upper or middle third. The average age of onset of ESCC is between the ages of 60 to 70 years and it is more frequently seen in males. It is usually asymptomatic until an advanced disease stage with common presenting symptoms being dysphagia (at first with solids then progressing to fluids) and weight loss. Less commonly odynophagia, hoarseness of voice, coughing, or chest pain can be presenting features. Source : https://www.orpha.net/en/disease/detail/99977 ) . However, it remains difficult to predict which patients will respond favorably to it. Faced with this major challenge, the gut mycobiota appears to offer hope, a Chinese study having found that gut fungal signatures may serve as biomarkers.

Partially repaired dysbiosis

An analysis of fecal samples showed that 68 ESCC patients had a significant dysbiosis of the gut mycobiota prior to treatment compared to 19 healthy controls: reduced diversity, higher abundance of pathogenic fungi and lower presence of beneficial fungi, and less complex ecological networks, indicating fewer synergies. Treatment with neoadjuvant immunochemotherapy improves the diversity and richness of the fungal community and rebalances certain beneficial metabolic pathways, although without reaching the levels seen in healthy subjects.

A mycobiota that predicts success

Most importantly, the profiles of the mycobiota sampled prior to treatment make it possible to distinguish future responders from non-responders. Responders have higher fungal diversity before treatment, more stable networks, suggesting greater resilience, and higher abundance of beneficial fungi (including Candida boidinii) correlated with “hot” tumor signatures (stimulation of T-helper 1 cells, pro-inflammatory cytokines, elevated cytotoxic markers).

What about non-responders? Their mycobiota was enriched in immunosuppressive species associated with characteristics of “cold” tumors (Th-2 cells, immunosuppressive cytokines).
Thus, the mycobiota of responders appears to promote immunity that contributes to tumor phenotypes favorable to the success of immunotherapy, while that of non-responders may contribute to tumor microenvironments that are resistant to immunotherapy.

Predict... and modulate response to treatment

Lastly, the mycobiota appears to be able to accurately and robustly predict future treatment efficacy, with the area under the curve (sidenote: Area under the curve (AUC) Indication of the discriminatory power of a classification model, for example, an AUC of 1.0 indicates a perfect classifier. It is the probability that the classification model will correctly classify a positive sample. ) reaching 82.9% (genus-level) and even 87.4% (species-level). The Saccharomyces genus appears to be the most robust predictor of non-response. These results suggest that the gut mycobiota may ultimately serve as a biomarker for stratifying patients in ESCC treatment.

Another potential application? Optimizing the results of immunotherapy, with the fungi identified, whether beneficial or harmful, representing targets for modulating the microbiota. The researchers’ initial findings show that administration of Candida boidinii enhanced the efficacy of anti-PD-1 therapy in mice. Could beneficial fungi one day improve treatment responses in patients with ESCC?

Ethanol, which can cross the blood-brain barrier (BBB), can damage the central nervous system. But it could also alter this barrier that protects our brain. A pathological process in which the gut-brain axis is involved, according to research published at the end of 2025 ¹.

The flora of alcoholics

Researchers analyzed the gut microbiota of 30 men who had suffered from alcohol use disorder (AUD) for years, and 30 control subjects. Compared to the control subjects, men with AUD showed cognitive impairment and signs of anxiety, depression, and sleep disorders. Their gut microbiota showed no significant differences in terms of abundance and diversity. However, the composition of their flora was specific: alcohol use disorder was associated with a decrease in Faecalibacterium and an increase in Streptococcus, a bacterium associated with inflammation.

Microbial metabolites present in plasma are also disrupted in cases of AUD: 604 metabolites were overexpressed (particularly in pathways related to lipid metabolism, amino acid metabolism, and bile acid secretion) and 606 were underexpressed. These variations were linked to the abundance of certain bacteria, such as Faecalibacterium.

Alcohol or fecal transplantation, same consequences in mice

The authors also show that chronic alcohol consumption leads to cognitive decline and BBB impairment in mice, with the appearance of leaks in the prefrontal cortex and hippocampus and a decrease in the expression of tight junction proteins in endothelial cells.

But above all, a simple fecal transplant from patients with AUD to axenic mice is enough to cause the same effects.The alteration of the gut microbiota caused by alcohol would therefore be partly responsible for the disruption of the BBB.

The restorative effect of Faecalibacterium prausnitzi

Since Faecalibacterium is less abundant in AUD patients, researchers tested whether F. prausnitzii could protect mice from brain disorders caused by chronic alcohol consumption. And indeed it does: cognitive function is improved, BBB leakage is reduced, and junction proteins are boosted.

Physiologically, F. prausnitzii led to a significant increase in certain short-chain fatty acids (butyric acid, valeric acid, and caproic acid) known for their anti-inflammatory effects. It therefore appears that this bacterium can protect the BBB from ethanol damage through the action of beneficial bacterial metabolites.

We know that alcohol can damage the brain. But did you know that it could also weaken the barrier that protects the brain from “intruders” coming from the blood? This protection, called the blood-brain barrier, is a bit like a safety net for our gray matter. And surprise: our gut seems to be playing a role in this scenario.

A microbiota not so innocent

Chronic alcoholics not only have problems with memory and concentration, but also with anxiety, depression and sleep disorders. Their gut microbiota is also suffering: Faecalibacterium, an anti-inflammatory bacterium, is less present, while Streptococcus, an inflammatory bacterium, is taking advantage of the situation to set up shop. And that’s not all: the blood plasma of alcoholic men is very different from that of men who are not addicted to drinking, with more than 600 molecules in excess and just as many in deficit. In short, an alcohol use disorder disrupts the gut microbiota, the composition of the blood and the functioning of the brain.

When the brain leaks... literally

To better understand the underlying mechanisms, mice were given alcohol for several weeks. The result: chronic alcohol consumption makes the barrier protecting their noggin permeable; leaks appear in key areas, and proteins essential to the integrity of the blood-brain barrier are down.

More surprisingly, transferring the intestinal microbiota of alcoholic patients to germ-free mice that do not drink alcohol is enough to induce the same type of brain leaks. Thus, the alteration of the intestinal microbiota caused by alcoholism is responsible for the disruption of the blood-brain barrier.

Faecalibacterium prausnitzii, the savior?

Since the friendly bacterium Faecalibacterium is missing in alcoholics, the researchers tested whether it could protect mice. Bingo! A few doses of Faecalibacterium prausnitzii allow mice to regain better cognitive abilities and their brain leaks less. How can a gut bacterium protect the barrier that surrounds the brain? Probably through the small anti-inflammatory fatty acids it produces in our digestive system, which slip into the bloodstream and thus reach the brain. Could F. prausnitzii protect against the damage caused by alcoholism? Maybe, although many other studies are still needed, this study ³ having been conducted only in men (not women) and mice. In any case, alcohol remains a substance to be consumed in moderation.

Will it one day be possible to predict the risk of pancreatic cancer using a simple oral swab? This may certainly be the case, according to a new study published in JAMA Oncology ¹. The study suggests that an imbalance in certain fungi and bacteria in our mouths may well be responsible for this cancer.

To demonstrate this, the authors used the medical records and oral microbiota samples of 122,000 individuals monitored over nine years, 445 of whom developed pancreatic cancer. 

Certain bacteria associated with increased risk

First, they discovered that the presence in the mouth of three bacteria involved in gingivitis and periodontitis (Porphyromonas gingivalis, Eubacterium nodatum, and Parvimonas micra) was associated with a higher risk of pancreatic cancer.

Whole-genome sequencing of oral microbes allowed the team to identify a total of 13 bacterial species linked to an increased risk, while 8 appeared to have a protective effect.

Key role of Candida fungi

The study was not limited to bacteria: the long-overlooked fungal microbiota was also analyzed. The researchers found that a greater abundance of Candida, the most common fungus in the oral cavity, is significantly associated with an increased risk of pancreatic cancer.

The researchers also observed that Candida fungi are found in tumor tissues, supporting the hypothesis of a migration of this microorganism from the mouth to the pancreas.
 

Towards a predictive biomarker

By combining all the microbial species identified, the researchers developed a microbial risk score. They found that each increase of one standard deviation in this score is associated with a nearly 3.5-fold increase in the risk of pancreatic cancer.

Taken together, these results strongly suggest that the oral microbiota is indeed involved in the development of pancreatic cancer. 
Could better oral health therefore help prevent this form of the disease? Further research will be needed to find out.

In any case, the oral microbiota could one day serve as a simple, non-invasive biomarker for the early identification of people most at risk of this deadly cancer. 
 

Pancreatic cancer remains one of the most deadly cancers, with a five-year survival rate of around 13%. Established risk factors (smoking, obesity, pancreatitis, and genetics) account for only 30% of cases.

Several epidemiological studies have shown that poor oral health, particularly the presence of periodontal disease and oral candidiasis, is associated with this cancer. Despite this, our knowledge about the actual involvement of oral microorganisms remains limited.

A large-scale prospective study using cohorts from the American Cancer Society Cancer Prevention Study-II and the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, has recently revealed that the oral microbiota, particularly bacteria and fungi, may play a significant role in the subsequent development of pancreatic cancer.

Periodontal bacteria: a strong link

Of the 122,000 participants who provided an oral sample, 445 developed pancreatic cancer during nearly nine years of follow-up. The researchers matched them with 445 healthy individuals to compare their oral microbiota.

The results published in JAMA Oncology ¹ show that three major pathogenic bacteria known to be involved in periodontal disease (Porphyromonas gingivalis, Eubacterium nodatum, Parvimonas micra) significantly increase the risk.

A comprehensive analysis of bacterial genomes revealed that a total of 21 species influence the risk of pancreatic cancer, some protective, others harmful. These taxa are thought to be associated with metabolic pathways that may promote the neoplastic transformation of pancreatic cells during their migration from the mouth to the pancreas.

Candida at the forefront

An analysis of the oral fungal microbiota—a parameter rarely explored in this context—also revealed that the genus Candida is associated with an increased risk of pancreatic cancer.

Candida tropicalis and Candida spp are associated with an increased risk, while C. albicans shows an inverse relationship. Within the Malassezia genus, only M. globosa was associated with cancer, and its effect was protective.

The researchers also report having confirmed the presence of Candida in biological samples of cancerous pancreatic tissue in cancer patients. This again supports the hypothesis of a migration of this fungus to the tumor and a direct role in carcinogenesis.

Towards early diagnosis and a better understanding of risk factors

In order to assess the impact of these microorganisms as a whole, the researchers calculated a Microbial Risk Score (MRS) for each participant, incorporating 27 bacterial and fungal species associated with cancer. They found that each increase of one standard deviation in the MRS more than triples the risk of pancreatic cancer (odds ratio [OR] 3.44).

According to the authors, the MRS score was reproducible between the two cohorts, suggesting the oral microbiota could one day be used as a biomarker in primary prevention to screen high-risk patients.

More generally, the data from this study reinforce the hypothesis that oral health is an important factor in the prevention of pancreatic cancer. Now we must try to better understand how oral fungal and bacterial communities promote cancerization processes.

To be continued...

We often conceptualize antimicrobial resistance (AMR) as a direct consequence of antibiotic overuse. However, a compelling new study published in npj Antimicrobials & Resistance shifts this paradigm, revealing that common "non-antibiotic" medications, drugs your patients likely take daily, may be silent drivers of this global health crisis, particularly in aged care settings ¹.

The hidden drivers in the medicine cabinet

We know that the gut microbiome is a complex ecosystem. Researchers examined how Escherichia coli, a common gut inhabitant and pathogen, responds to nine widely used non-antibiotic medications (NAMs) commonly prescribed in Residential Aged Care Facilities (RACFs), including ibuprofen, acetaminophen (paracetamol), and atorvastatin. The scientists from the University of South Australia didn't just dump drugs on a petri dish; they modeled specific "gut-relevant concentrations" to mimic the actual physiological environment of a patient taking these medications orally.

It appears that these drugs are not biologically inert regarding bacterial evolution. While they don't kill the bacteria like antibiotics do, they exert a stress that fundamentally changes bacterial behavior. Specifically, the study focused on whether these common drugs could enhance mutagenesis (sidenote: Mutagenesis The biological process by which the genetic information of an organism is changed, resulting in a mutation. ) when the bacteria were also exposed to ciprofloxacin, a fluoroquinolone antibiotic frequently used for UTIs in the elderly.

When painkillers mimic antibiotics

The most potent drivers of resistance weren't the obscure drugs, but the everyday painkillers. The data showed that ibuprofen and acetaminophen significantly increased the mutation frequency in E. coli. When exposed to these analgesics alongside ciprofloxacin, the bacteria developed high-level resistance much faster than with the antibiotic alone.

The mechanism uncovered is both sophisticated and alarming. Researchers utilized whole genome sequencing (sidenote: Whole genome sequencing A comprehensive laboratory method used to determine the complete DNA sequence of an organism's genome. Researchers utilized this technique to pinpoint specific mutations in resistance genes like GyrA, MarR and AcrR. ) to pinpoint key mutations: not only in the antibiotic's target, the GyrA gene (sidenote: GyrA gene A gene that encodes a specific subunit of the DNA gyrase enzyme, which acts as the primary biological target for fluoroquinolone antibiotics like ciprofloxacin. Mutations in this gene can prevent the antibiotic from binding effectively, leading to resistance. ) , but significantly, in MarR and AcrR, the regulatory genes controlling efflux pumps (sidenote: Efflux pumps Cellular transport proteins (specifically AcrAB-TolC in this context) that bacteria use to actively expel toxic substances from within the cell. The text describes them as acting like an internal "bilge pump" to flush out both the medication and the antibiotic. ) . Critically, the presence of common analgesics like ibuprofen or acetaminophen was found to induce the bacteria to overexpress the AcrAB-TolC efflux pump. This action is akin to the bacteria activating an internal "bilge pump" to expel the medication, which simultaneously flushes out the antibiotic and, disturbingly, solidifies genetic resistance.

The polypharmacy multiplier

The study went a step further to simulate "polypharmacy (sidenote: Polypharmacy The simultaneous use of multiple medications by a single patient. This practice is common in aged care settings and was shown to significantly increase the level of antibiotic resistance in bacteria exposed to drug combinations. ) ", or the use of multiple drugs, which is standard for many elderly patients. When E. coli was exposed to two NAMs simultaneously (like ibuprofen plus diclofenac), the results were striking. While the frequency of mutations didn't necessarily explode, the level of resistance did. Some mutants exhibited a staggering 64-fold increase in ciprofloxacin resistance compared to the wild type. This suggests that the "cocktail" of medications standard in aged care may be creating a perfect storm for evolving "superbugs". The takeaway for us isn't to stop prescribing pain relief, but to view these medications with new respect. They are active participants in the microbial environment, capable of accelerating resistance mechanisms that threaten public health.
 

We usually think of antibiotic resistance as a war fought only with antibiotics. The logic is familiar: if you overuse them, the surviving bacteria adapt into "superbugs". But a groundbreaking new study reveals that this view is incomplete.

Research published in npj Antimicrobials & Resistance ¹ shows that the everyday medications in your cabinet, specifically non-antibiotic drugs like ibuprofen and acetaminophen, are active participants in your gut’s ecosystem. Surprisingly, they may be training bacteria to resist antibiotics, even when you aren't taking any antibiotics at all.

The surprise in your medicine cabinet

Researchers at the University of South Australia examined how Escherichia coli, a common gut bacterium, responds to standard non-antibiotic medications. They didn't just pour drugs on a dish; they carefully modeled "gut-relevant concentrations" to mimic exactly what happens in your body after swallowing a pill.

The findings were striking. While these drugs don't kill bacteria, they stress them. The study found that common painkillers, ibuprofen and acetaminophen (paracetamol), significantly increased the rate at which E. coli mutates. When these bacteria were later exposed to ciprofloxacin (a standard antibiotic), they evolved resistance much faster than bacteria that hadn't encountered the painkillers.

The "bilge pump" mechanism

How does a painkiller block an antibiotic? The mechanism is elegant and scientifically fascinating. The researchers found that these drugs flip specific genetic switches inside the bacteria.

These switches turn on what is called an efflux pump (sidenote: Efflux pumps Cellular transport proteins (specifically AcrAB-TolC in this context) that bacteria use to actively expel toxic substances from within the cell. The text describes them as acting like an internal "bilge pump" to flush out both the medication and the antibiotic. ) . Think of this like a bilge pump on a leaking ship. The bacteria sense the chemical stress of the painkiller and start pumping furiously to flush it out. The problem? This pump is non-specific. Once activated, it doesn't just eject the painkiller; it mechanically flushes out antibiotics too. 

The "cocktail effect"

The study also simulated taking multiple medications at once, which is common for older adults. When bacteria were exposed to two non-antibiotic drugs simultaneously (like ibuprofen plus diclofenac), the danger shifted.

While the number of mutants didn't necessarily explode, the strength of their resistance did. Some mutants from these drug cocktails developed a staggering 64-fold increase in resistance compared to normal bacteria. This means the bacteria weren't just resistant; they were practically immune to standard antibiotic treatments.

This isn't a reason to panic or stop taking necessary medication. However, it changes how we view our bodies. Your gut is an adaptive environment, and common drugs act as biological inputs that can inadvertently toughen up bacteria. Understanding this helps us use these tools more wisely.

During unprotected sex, thousands of microorganisms are also shared via semen and vaginal secretions. Yet for years, researchers have scrutinized the vaginal microbiota (which has been extensively studied) on the one hand, and the semen microbiota (which has been studied much less) on the other, as if they lived on two different planets. The idea that they might interact in a sexually active couple? Barely touched upon by 14 small studies.

Two very different worlds, but open to exchange

The seminal microbiota of men is completely different from the vaginal microbiota of women: it is generally more diverse, has a lower bacterial concentration, and a slightly alkaline pH of 7.5... whereas the vaginal microbiota is less diverse, dominated by lactobacilli, and has an acidic pH (a direct consequence of the abundance of lactobacilli, which secrete acids) .

However, unprotected sex means the exchange of fluids and bacteria. Female couples often share a similar vaginal microbiota. Male homosexual couples (men who have sex with men) are distinguished by a unique rectal microbiota, rich in Prevotella and less diverse than that of heterosexual men.

In heterosexual couples, these exchanges could have consequences for fertility. This is true for both women and men. For example, an increased abundance of Lactobacillus in the seminal microbiota would go hand in hand with more mobile and concentrated sperm, but also—on the flip side—an adherence of lactobacilli to sperm that would reduce fertility.

STIs and dysbiosis also on the menu

Unprotected sex contributes to the transmission of sexually transmitted infections (STIs) but also disrupts the balance of intimate microbiota (dysbiosis (sidenote: Dysbiosis An imbalance in the microbial community, characterized by reduced beneficial bacteria and increased harmful species, potentially leading to adverse health outcomes. ) ).

Take, for example, the dreaded bacterial vaginosis, linked to a decrease in Lactobacillus and an increase in bacteria such as Gardnerella vaginalis. In heterosexual women, the increase in vaginal pH induced by semen could be a triggering factor for imbalance. It is also important to note that circumcision alters the microbiota of the penis skin, reducing its diversity and the presence of bacteria associated with bacterial vaginosis. Whether this protects women is still a matter of scientific debate.

Assisted reproduction

The microbiota in semen and the vagina may also play a role in the outcome of IVF (sidenote: In vitro fertilization (IVF) A medical assistance technique for procreation where fertilization takes place in the laboratory, in a test tube (“in vitro”), and not in the woman’s uterus: eggs retrieved from the woman after hormonal stimulation are placed in a nutrient solution with sperm collected from the man. The embryos thus conceived in the laboratory will then be transferred to the future mother’s uterus via the vagina. If an embryo implants, the pregnancy begins. https://www.service-public.fr/particuliers/vosdroits/F31462
https://medclinics.com/fr/fiv/
https://www.fiv.fr/fecondation-fiv/ ) , with certain seminal (Acinetobacter) or vaginal (L. crispatus) bacteria being associated with a higher chance of success. Conversely, Prevotella and Porphyromonas bacteria in parents reduce the chances of success.

A couple's reproductive health therefore appears to be linked to the so-called semivaginal (sidenote: Microbiote séminovaginal L’ensemble des micro-organismes provenant des écosystèmes séminal et vaginal qui sont transférés et partagés entre les partenaires lors de rapports sexuels non protégés, s’influençant mutuellement et impactant la santé et les fonctions reproductives. ) microbiota, which is still largely unknown. It is high time to gain a better understanding of how these microbiotas interact, coexist, and sometimes clash. Because yes, in a couple, intimate microbiotas also share a life together.

Serotonin is essential to the digestive system: it regulates essential gastrointestinal functions (peristalsis, vasodilation, visceral sensitivity) and promotes the development and maintenance of the enteric nervous system. Although serotonin production is mainly endogenous (in two stages: tryptophan -> 5-HTP -> serotonin), certain human enteric bacteria are suspected of contributing to it. Scientists have recently identified these bacteria and evaluated the physiological activity of this microbial serotonin on colonic innervation and intestinal motility.

Serotonin-producing lactobacilli

The results confirm that the gut microbiota synthesizes serotonin and contributes to intestinal levels of this substance: in vitro (anaerobic cultures), the human fecal microbiota of healthy volunteers produces serotonin; in vivo, serotonin is found in the stools of mice that are genetically incapable of synthesizing it once they are given microbiota. Which bacteria are responsible? Researchers have identified a pair of serotonin-producing lactobacilli (named Ls), consisting of Ligilactobacillus ruminis and Limosilactobacillus mucosae. Ls does not produce 5-HTP or serotonin from tryptophan (step 1 of synthesis), but produces serotonin in the presence of 5-HTP (step 2). This step 2 of decarboxylation of 5-HTP to serotonin requires the simultaneous presence of both bacteria in the consortium.

Effects of intestinal colonization by the bacterial duo

In axenic mice unable to produce endogenous serotonin, colonization by Ls strains alone increases entero-serotonin levels, promotes colonic innervation, and increases the number of serotonin-immunoreactive neurons. However, serum serotonin levels in mice are unchanged, suggesting that bacterial serotonin primarily regulates local intestinal functions.

The isolated Ls community produces serotonin in vitro. However, this effect is not reproduced in culture conditions with pure strains (L. mucosae or L. ruminis) or with their reconstituted co-culture, whereas this co-culture increases fecal serotonin in vivo. This suggests that microbial serotonin production may depend on specific intestinal conditions (substrates, pH, oxygen, cofactors, microbial interactions).

Restoring patients' intestinal motility?

Finally, Ls normalizes intestinal transit time in axenic mice. However, in patients with irritable bowel syndrome, the fecal abundance of L. mucosae (but not L. ruminis) is significantly lower than in healthy controls. And the less this bacterium is present, the harder the stools are. Could a mechanism linked to the microbiota affect local serotonin biosynthesis and intestinal motility in these patients? According to the authors, future research could determine whether these serotonin-producing bacteria are capable of restoring physiological serotonin levels in patients with intestinal motility disorders.