The findings, published in Nature, suggest that early social interactions, especially among nursery peers, help to build and diversify the infant gut microbiota.

Previous studies showed that microbes are shared between peers, suggesting that nurseries may shape infant microbiotas through baby-to-baby transfer. However, not much is known about how babies’ microbiotas change once they begin interacting with other children.

Liviana Ricci at the University of Trento in Italy and her colleagues followed 43 babies during their first year of nursery and tracked how their gut microbiotas changed over time.

Similar microbiotas

The researchers collected and analyzed more than 1,000 stool samples from babies, family members, caregivers, and household pets. The team confirmed expected differences between adult and baby microbiotas, and showed that babies’ microbial diversity increased over time, especially as they attended nursery. 

Babies shared many microbial strains with their mothers at the start of the study, and people living in the same family also shared more strains with each other than with unrelated individuals. 

Babies with siblings tended to have more diverse microbiotas, and factors such as birth method or antibiotics at birth no longer had a strong effect on gut microbes by about 10 months of age. As babies spent time together in nurseries, their microbiotas became more similar to each other, the researchers found.

Building microbiotas

Using genetic tracking, the researchers were able to reconstruct bacterial strains passing from a baby to another baby in the nursery and then spreading to that child’s parents at home. They also found a few examples of microbes being shared between babies and pets.

Within a few months, bacteria acquired from nursery peers made up a larger share of babies’ microbiotas than those from family members. Even after long breaks, such as summer vacation, babies continued to share more microbes with former nursery peers than with children from other nurseries, the researchers found.

“Overall, our results reveal the centrality of social factors in shaping the infant microbiome via inter-individual microbial transmission, thus rebalancing social interactions as key to building a healthy microbiome,” they say.

This study, published in Nature Communications mapped early-life patterns of microbial conjugated bile acids (MCBAs) and their connection to islet autoimmunity.

Bile acids (BAs), derived from cholesterol and produced in the liver, play crucial roles in lipid absorption and signaling in the gut. They are modified by gut microbes into a variety of secondary BAs, with a significant portion recirculated to the liver through enterohepatic circulation. Recent findings indicate that gut microbes can also reconjugate BAs, leading to the identification of MCBAs. These compounds interact with various receptors, influencing metabolism and immune responses. Dysregulated BA levels are linked to several diseases, including type 2 diabetes and inflammatory bowel disease. 

This longitudinal study aims to explore the trajectories of MCBAs in relation to islet autoimmunity and type 1 diabetes of children (n= 74, 3-36 months) through collection of stool samples (n=303). The study focuses on children who developed multiple autoantibodies, single autoantibodies, and those who remained negative for autoantibodies, as well as the interplay between MCBAs and gut microbiota.

A total of 110 MCBAs were examined, revealing how:

• 78 present in at least one sample, with primary bile acids (CA, Chenodeoxycholic Acid, CDCA) being more prevalent than secondary (Deoxycholic Acid, DCA; Ursodeoxycholic Acid, UDCA; Hyodeoxycholic Acid, HDCA)
• Various factors influenced MCBA profiles being the age  the primary determinant affecting 48 MCBAs
• After the first year, primary BA amidates declined, while secondary BA amidates increased, stabilizing or slightly decreasing by 24 to 36 months. Different trends were noted for HDCA conjugates, with some decreasing and others increasing with age. 
• Nine MCBAs differed by sex, and three were associated with breastfeeding duration, indicating the complexity of early-life bile acid metabolism

MCBAs and islet autoimmunity

Concentrations of ten MCBAs differed significantly between children who developed islet autoantibodies (P1Ab and P2Ab groups) and the controls. Notable findings include:

• Lower DCA conjugates in the P1Ab group compared to controls, while CDCA-Tyr showed an opposing trend
• Different age cohorts demonstrated inconsistencies in MCBA profiles across time points, yet specific conjugates remained significantly altered, with only UDCA-Asn consistently lower in the P2Ab group at 12 months
• Bacterial communities correlated with altered BA profiles, especially DCA conjugates, identifying 72 bacterial strains with associations to these metabolites, such as Eubacterium eligens and Bacteroides fragilis. Indeed, numerous microbial strains were found capable of producing specific MCBAs, supporting the role of gut bacteria in BA metabolism and their potential influence on islet autoimmunity development.

MCBAs modulate host immune responses

MCBAs were investigated for their immunomodulatory effects on the innate immune system, focusing on responses to lipopolysaccharide (LPS) in human whole blood cultures showing: 

• Various bile acid conjugates displayed different impacts on LPS-induced signaling pathways downstream of the TLR4 receptor, with unconjugated UDCA and certain conjugates inhibiting signaling, while others enhanced it
• Examining the effects of MCBAs on the adaptive immune system during the differentiation of Th17 and iTreg cells it was showed how UDCA-Asn and CDCA-Ser promoted Th17 differentiation and IL-17a secretion, while inhibiting iTreg cell differentiation
• Unconjugated UDCA and CDCA-Tyr did not affect iTreg populations but reduced IL-17a secretion, inhibiting Th17 differentiation
• RAR-related orphan receptor alpha (RORα) expression in Th17 cells appeared to correlate with IL-17A levels following treatment with these MCBAs, indicating a potential role in bile acid-mediated modulation of immune responses

To summarise, this study track microbially conjugated bile acids through early childhood, revealing their key role in islet autoimmunity development. Not only. These gut bacteria-modified bile acids strongly correlate with microbiome composition and actively shape the balance between pro-inflammatory Th17 and regulatory Treg immune cells — positioning MCBAs as crucial influencers of immune development.

In this closing interview from PPPP 2026 in Lecce, Prof. Flavia Indrio reflects on the main take-home messages from the congress, which brought together 32 leading international experts in microbiota research, allergy, nutrition, gut-brain axis and lung disease. Among the strongest themes to emerge was the importance of early-life intestinal colonization, with breastfeeding, avoidance of unnecessary C-sections and prompt management of dysbiosis identified as key factors in shaping health trajectories later in life. Indrio also highlights the growing clinical relevance of gut-brain axis research, which is beginning to open new therapeutic perspectives in severe pediatric conditions such as autism spectrum disorders and cognitive development disorders. 

A central focus of her interview is a 10-year follow-up study on newborns supplemented with Lactobacillus reuteri during the first three months of life, showing that beneficial effects may persist over time. The interview also touches on new insights into allergy, the interplay between microbiome and epigenetics, and the pivotal role of nutrition as a driver of intestinal colonization. The next PPPP meeting, she announces, will take place in Mexico City in March 2028, with broader involvement from the Latin American scientific community.

The findings, published in Cell Host & Microbe, suggest that supporting maternal gut health and optimizing breast milk composition could help shape healthy infant gut development.

Breast milk is known to provide not only nutrients but also human milk oligosaccharides (HMOs)—complex sugars in breast milk that feed beneficial gut bacteria such as Bifidobacterium, which initially dominate the infant microbiota. However, it remains unclear how maternal gut microbes, breast milk composition, and infant gut microbes interact over time.

To address this question, researchers led by Lishi Deng at Ghent University in Belgium followed 152 mothers and their babies in rural Burkina Faso.

Microbiota profiles

The team collected maternal stool samples during pregnancy, breast milk samples from 2 weeks to 4 months, and infant stool samples at 1-2 and 5-6 months. Almost all infants were exclusively breastfed for about six months. 

The infant gut was initially dominated by helpful bacteria such as Bifidobacterium and Escherichia, while mothers’ guts and milk contained much more diverse microbial communities. 

Early on, infants fell into three distinct gut microbiota profiles—Bifidobacterium-dominant, Escherichia-dominant, and pathogen-rich. By six months, however, these differences disappeared and the infant gut communities became more diverse. Breast milk composition also changed: early milk was richer in certain sugars, proteins, vitamins, and minerals that declined over time, the researchers found.

Two-way interaction 

Differences in mothers’ gut microbes during the third trimester of pregnancy were associated with distinct gut microbiota patterns in infants at 1-2 months of age. For example, mothers whose babies had a Bifidobacterium-rich gut profile at 1-2 months tended to produce higher levels of HMOs. Later, at 5–6 months, other breast milk nutrients—such as iron, vitamins, and minerals—became more important than HMOs.

The researchers also found evidence that an infant’s early gut microbes were linked to changes in milk composition months later, suggesting that babies may influence the milk they receive.

The findings, the authors say, “offer insights into early-life microbial development and inform future mechanistic studies and microbiome-targeted interventions, particularly in low-resource settings.”

The findings, published in Nature Communications, may inform strategies to improve early-life gut health as well as infant nutrition and disease prevention.

Scientists have known that breast milk contains some bacteria that can influence the infant gut microbiota, but the detailed composition of the breast milk microbiota and which specific bacterial strains are shared with the infant gut remain unclear.

So, Pamela Ferretti at the University of Chicago in Illinois and her colleagues analyzed breast milk and infant stool samples from 195 mothers and their babies, most of whom were exclusively breastfed during their first six months.

Shared microbes

The researchers found that although the types of bacteria in milk and baby stool are different, both are dominated by Bifidobacterium longum. Breast milk included other Bifidobacterium species, skin bacteria, and mouth bacteria, while babies’ guts were dominated by Bifidobacterium species and some gut and oral bacteria.

From one to six months of age, B. longum became more common in the guts of babies, especially those who were exclusively breastfed, while other bacteria such as E. coli decreased. The presence of B. longum was linked to a more stable gut microbiota over time, the researchers found.

About 10% of the bacteria in a one-month-old baby’s stool were also found in their mother’s milk. Besides B. longum, other bacteria such as B. bifidum, E. coli, and some oral microbes were most frequently passed from milk to infant gut. Some of these strains persisted in the baby’s gut for several months.

Antimicrobial resistance

Further analyses revealed that both breast milk and infants’ gut bacteria harbor genes that allow them to produce essential nutrients such as amino acids. Both milk and infant guts also contain genes that provide resistance to antibiotics. 

Some antimicrobial resistance genes were shared between a mother’s milk and her baby’s gut, and babies whose guts were dominated by Bifidobacterium had fewer resistance genes, the researchers found.

“Our results indicate that maternal breast milk plays a role in infant gut microbiome and resistome establishment, development, and temporal stability,” the authors say. The work, they add, als offers a detailed picture of the bacteria in breast milk and how they relate to the bacteria in a baby’s gut, providing better information for future research.

The findings, published in Cell Host & Microbe, suggests that dietary fiber is a potential fertility-support strategy.

Recent research has indicated that the microbiota plays a key role in reproduction by supporting growth, development, and egg production. In humans, changes to the microbiota caused by antibiotics, diet or conditions such as obesity are linked to reproductive problems, but the exact reasons remain unclear. 

Sarah Munyoki at the University of Pittsburgh School of Medicine in Pennsylvania and her colleagues set out to examine how gut microbes and diet during early life affect fertility in mice.

Ovarian health

In normal mice, the gut microbiota shifts after birth, especially during weaning, becoming richer and more complex. Early on, the gut is dominated by bacteria adapted to breast milk, but after weaning, microbes that break down solid food and produce beneficial compounds such as short-chain fatty acids (SCFAs) expand. Female mice raised without gut microbes showed disruptions in ovarian development that coincided with this microbiota transition, the researchers found.

Compared to mice with a healthy microbiota, female mice raised without microbes had fewer litters and fewer pups per litter, and they stopped reproducing earlier in life. By puberty, germ-free mice began losing follicles much faster than mice with a healthy microbiota, with poor progression to later stages and higher rates of follicle death. 

The ovaries of germ-free mice showed damage, with signs of tissue scarring. Genetic analysis revealed that key genes for maintaining and activating ovarian follicles—the reserve needed for producing eggs—were less active than in mice with a healthy microbiota.

Improving fertility

Giving germ-free female mice normal gut microbes either at birth  or at weaning restored the follicles to normal levels and reversed tissue damage. This recovery matched a return of normal gut bacteria diversity and production of SCFAs. Just giving germ-free mice SCFAs in drinking water starting at weaning rescued ovarian health, at least in part.

Finally, the researchers fed mice different diets starting at weaning. High-fat, low-fiber diets caused the biggest loss of ovarian follicles and altered ovarian gene activity, while adding fiber helped protect ovaries, even in high-fat conditions. Fiber also improved gut bacteria, boosted SCFAs levels, and reduced inflammation in ovaries. 

The findings suggest that dietary fiber during early life protects fertility by supporting healthy gut microbes and preventing ovarian damage caused by high-fat diets, the authors say. “Future studies should examine the relationship between diet, microbiota, and ovarian reserve in individuals with reproductive disorders and assess the efficacy of microbiota-directed interventions in improving fertility outcomes.”

Collecting the first clues

The search began with a simple but powerful idea: to explore the gut ecosystem in the earliest stage of life. Samples collected from 26 healthy babies, all breastfed and delivered naturally, became the starting point for this scientific journey. These infants, only a few months old, had guts still untouched by weaning or extensive environmental exposure, a pristine microbial landscape, a treasure trove for those who knew how to look.

Back in the laboratory, the samples became the raw material for a painstaking journey of isolation. Scientists plated them on selective media, incubated them under strictly controlled conditions, and examined the colonies that emerged. What might have looked like anonymous specks on agar plates soon revealed their identities under genetic sequencing: dozens of strains belonging to the familiar probiotic families of Lactobacillus and Bifidobacterium. From this microbial crowd, only a handful would pass the rigorous tests ahead.

The criteria were exacting. Any candidate strain had to survive the hostile environment of the human stomach, rich in acid and bile salts. It had to prove its ability to cling to intestinal cells, since without adhesion there could be no meaningful interaction with the host. Safety came next, particularly the absence of transferable antibiotic resistance genes. Finally, the strains were tested for their ability to influence immune cells, those sentinels of the body that decide whether to tolerate, resist, or respond. Each step was a hurdle, and many promising candidates fell by the wayside.

Three probiotic protagonists emerge

Out of this arduous selection process, three names began to stand out: Bifidobacterium breve 2TA, Lacticaseibacillus rhamnosus L13B, and Lactobacillus gasseri L6. Each strain, property of Coree srl, brought to the table a different kind of strength, and together they illustrated the diversity of probiotic potential hidden in the microbiome of infants.

• Bifidobacterium breve 2TA distinguished itself in its dialogue with the immune system. When exposed to human dendritic cells in vitro, this strain promoted their maturation and influenced cytokine production, tilting the immune balance toward a more active state. Though Bifidobacterium strains often struggle to withstand the harsh chemistry of the stomach, 2TA showed that survival is not the only metric of value; its ability to interact with the immune system suggested a role as a subtle but powerful modulator in the infant gut.
• Lacticaseibacillus rhamnosus L13B, on the other hand, excelled where persistence and growth mattered. It demonstrated a robust capacity to adhere to intestinal cells, ensuring it could remain in place long enough to act. Even more intriguingly, it grew successfully in reconstituted skimmed milk, hinting at the possibility of incorporation into dairy-based functional foods. Its immune profile was equally notable, stimulating pro-inflammatory cytokines such as IL-1β and TNF-α, responses that might be useful in enhancing defenses against pathogens during early life.
• Then came Lactobacillus gasseri L6, perhaps the most resilient of the trio. Unlike many strains that faltered when faced with simulated gastric transit, L6 survived with little loss of viability. It also showed one of the highest levels of adhesion to intestinal cells, positioning itself as a hardy colonizer. In immune tests, it modulated certain co-stimulatory molecules, although its effect was more modest than that of its counterparts. Still, its endurance marked it as a strain capable of real persistence in the gut environment, a quality indispensable for long-term probiotic action.

Together, these three strains represented more than just new microbial names. They illustrate a broader concept: probiotics are not interchangeable entities but unique biological actors, each defined by its own metabolic and immunological profile. Their discovery reinforces the idea that the future of probiotic science lies in precision, identifying strains that match specific physiological needs or life stages.

Beyond the Petri dish: the promise of personalized probiotics

The story does not end here. For now, the evidence rests on in vitro characterizations, a crucial first step but not the final proof of probiotic efficacy. The next chapters will need to be written in the form of clinical trials, safety validations, and perhaps the development of functional foods or infant formulas that bring these strains from Petri dish to everyday life. Yet even at this early stage, their story resonates as a reminder of how deeply connected we are to the invisible organisms that share our bodies, and how much remains to be discovered when we look at them with fresh eyes.

In the end, Bifidobacterium breve 2TA, Lacticaseibacillus rhamnosus L13B, and Lactobacillus gasseri L6 are not just bacteria: they are witnesses to the intimate, ancestral dialogue between mothers, infants, and microbes. They remind us that the quest for health sometimes begins not in distant laboratories, but in the very first days of life, carried quietly in the gut of a newborn.

The findings, published in Science, suggest that antibodies in breast milk are a key regulator of intestinal immune development in early life.

In newborns, breast milk provides antibodies along with nutrients and live bacteria. Studies in mice show that maternal antibodies, more than maternal immune cells, prevent excessive activation of gut immune cells, but the exact ways different types of antibodies work in early life are still unclear.

Meera Shenoy at Fred Hutchinson Cancer Center in Seattle, Washington, and her colleagues investigated how maternal antibodies in breast milk shape early-life gut immunity in mice.

Milk antibodies

Mice pups whose mothers lacked antibodies had higher numbers of certain immune cells in gut lymph nodes after weaning, indicating immune over-activation. 

In newborn mice, breast milk antibodies—especially one type called IgG—play a key role in regulating the gut immune system during the first week of life. Early milk is particularly rich in IgG, and even tiny amounts of IgG during the first week prevented over-activation of gut immune cells after weaning. Other milk components, including IgA antibodies, did not have this effect. 

Exposure to IgG antibodies during the first week of life protected the pups against conditions associated with gut inflammation, such as colitis, and also limited immune overreactions to new food antigens. However, later exposure to these antibodies couldn’t fully prevent immune dysregulation, the researchers found. 

Immune education

Experiments in germ-free mice and mice treated with antibiotics—which lack normal gut microbes—showed that this immune regulation depends on the presence of microbes, but it doesn’t require large changes in overall microbiota composition.

Further tests showed that IgG must bind to gut bacteria to be effective. IgG that bound microbes prevented immune over-activation in mice, while IgG that didn’t bind microbes could not. 

The findings show that maternal IgG in breast milk helps the gut immune system shape the microbiota, strengthen the gut barrier, and restrain inflammation, the researchers say. “Further understanding the maternal-offspring interactions that shape immune education will advance strategies to promote beneficial responses to innocuous microbes and environmental antigens and prevent pathological responses throughout life.”

The findings, published in Cell Reports, suggest that the maternal oral microbiota plays a key role in influencing infant gut health and disease risk.

Babies get much of their first gut bacteria from their mothers—through birth, breastfeeding, and close contact. These microbes come from various parts of the mother’s body, and if harmful bacteria are passed to the baby, they may raise the risk of gut inflammation and disease. However, how exactly these bacteria persist in the infant gut, and how they contribute to disease, is still unclear.

Researchers led by Masafumi Haraguchi at University of Michigan in Ann Arbor set out to investigate how mothers with an imbalanced mouth microbiota influence the community of gut microbes in their offspring.

Immune imprinting

The researchers caused gum disease in mother mice, which led to the growth of a harmful oral bacterium called Klebsiella aerogenes. This bacterium was passed to the mice’s pups and colonized their guts during the first weeks of life. However, the microbe disappeared as the pups’ guts became more diverse with age. 

Klebsiella aerogenes changed the pups’ immune environment in the gut, increasing certain immune cells that can cause inflammation. The early exposure to the bacterium also affected how genes related to inflammation and metabolism work in the gut, the researchers found.

Compared to pups born to healthy mothers, those born to mothers with oral infections showed worse symptoms and inflammation when their guts were challenged. This increased risk appears to come from the early “immune imprinting” caused by exposure to the mother’s oral bacteria. 

Mouth health

Even after the harmful bacteria disappeared as the pups grew, some immune imbalances persisted into adulthood, making the animals susceptible to gut inflammation. 

“Our results provide compelling evidence that maternal oral health, particularly the presence of oral dysbiosis, significantly influences the development of gut microbiota and the immune system in offspring, ultimately impacting health outcomes from infancy through adulthood,” the researchers say.

Although it’s unclear whether the effects observed in mice translate to humans, the authors add, the findings highlight the importance of good oral health in mothers during pregnancy and early childcare to support healthy gut development and prevent immune-related gut problems.

The findings, published in Nature Communications, suggest that breastfeeding and Bifidobacterium could offer strategies to reduce antibiotic resistance early in life.

Right after birth, babies begin to develop a community of gut microbes and a resistome—the collection of antibiotic resistance genes associated with those microbes. This process is shaped by factors such as birth method, feeding, and antibiotic use. Since early exposure to these genes can lead to serious health risks, understanding how the infant resistome develops is crucial for preventing long-term problems.

Anna Samarra at the Institute of Agrochemistry and Food Technology in Valencia, Spain, and her colleagues set out to examine how breastfeeding and the presence of Bifidobacterium bacteria influence the development of antibiotic resistance genes in infants during their first year. 

Antibiotic resistance

The researchers analyzed more than 265 stool samples from 66 mother-infant pairs. They found antibiotic resistance in every sample, with infants having more and a wider variety than their mothers, especially in the first week of life. 

Many of these antibiotic resistance genes, especially those related to resistance against tetracyclines and macrolides, were shared between infants and their mothers. In the first year of life, the total number of antibiotic resistance genes in infants decreased, and their gut bacteria and resistome became more similar to those of their mothers. 

Certain bacteria—such as Streptococcus, Staphylococcus, Escherichia, and Klebsiella—carried many of these resistance genes. However, diet and breastfeeding practices influenced which antibiotic resistance genes were present, the researchers found.

Window of opportunity

Infants with higher levels of Bifidobacterium bacteria in their guts during the first year of life tended to have lower levels of harmful bacteria such as Escherichia coli and Klebsiella, as well as fewer and less diverse antibiotic resistance genes. 

Exclusive breastfeeding was linked to higher Bifidobacterium levels and helped reduce antibiotic resistance genes, especially in infants born through a C-section, who had more antibiotic resistance genes.

The protective effects of breastfeeding appear to be strongest in the first month of life, suggesting that this period is a “window of opportunity” to support a baby’s microbiota and reduce antibiotic resistance, the authors say. “Establishing evidence that breastfeeding or components of human milk offer protection against colonization or infection with [antimicrobial resistant] bacteria would provide strong support for intensifying efforts to

advocate for breastfeeding through policy initiatives.”