The findings, published in Science Immunology, suggest that these intestinal cells, rather than immune cells, are the key sensors of beneficial microbes, helping maintain gut health and prevent inflammation.

Scientists have known that macrophages depend on signals from gut microbes to develop properly, and when this process fails, chronic diseases such as inflammatory bowel disease can occur. Although sensors called Toll-like receptors on the surface of immune cells help detect microbes, what guides macrophage recruitment is unclear.

So, researchers led by Ming-Ting Tsai at Baylor College of Medicine in Houston, Texas, set out to investigate how epithelial cells in the gut communicate with the immune system.

Activating immunity

The researchers found that colonizing mice with a specific strain of the commensal bacterium Escherichia coli, called 541-15, restored macrophages after antibiotic treatment. Mice with E. coli 541-15 were also protected against chemically induced colitis, showing less inflammation, longer colons, and lower disease markers than mice without the bacterium. 

E. coli 541-15, through its flagellin protein—which makes up the tail-like flagellum that the bacteria use to move, is sensed by a specific Toll-like receptor called TLR5 on epithelial cells that act like stem cells in the gut. These cells secrete molecules that attract immune cells, including macrophages. 

Using lab-grown “mini-colons” that mimic human intestinal tissue, the team discovered that mature colon cells did not respond to the bacteria, while the stem-like cells strongly activated genes involved in immune recruitment without causing inflammation. 

Microbial sensing 

Further experiments showed that E. coli 541-15 helps the colon recruit key immune cells that can develop into macrophages, leading to more mature, protective macrophages and fewer immature ones. 

This effect depended on a chemical signal called CCL2. When CCL2 was blocked or genetically removed from epithelial cells, mice were no longer protected against colitis, and fewer immune cells were recruited to the gut lining. E. coli strains with active flagellin activated TLR5 on epithelial cells, while strains without active flagellin didn’t.

It’s still unclear how these findings apply to humans, and whether other microbial signals help recruit immune cells to the gut, the authors say. However, they add, “our study demonstrates a role for intestinal epithelial stem cells in microbial sensing, which promotes intestinal macrophage replenishment and maturation and supports intestinal barrier function.”

The findings, published in Cell Host & Microbe, reveal a gut-testis interplay that may explain why low oxygen environments reduce male fertility at high altitudes.

In addition to low air pressure and oxygen levels, gut imbalances, diet, and microbial metabolites can also affect sperm. However, how gut changes at high altitudes cause sperm damage—and which bacteria and metabolites are involved—remains unclear.

So, researchers led by Jianchun Zhou at the Army Medical University in Chongqing, China, set out to study how sperm quality is affected by high-altitude low-oxygen conditions.

High-altitude conditions

In experiments with mice, males living at the equivalent of 5,800 meters produced fewer pregnancies when mated, had smaller testes, lower sperm concentration and motility, and showed structural damage in the sperm-producing tubules compared to males living at lower altitutdes. 

High-altitude low-oxygen conditions increased the levels of a bacterium called Clostridium symbiosum, which produces a metabolite called succinate. Giving mice either C. symbiosum or succinate lowered sperm quality, while a modified version of the bacterium that cannot make succinate did not. 

Succinate travels from the gut to the testis and harms sperm development by activating a type of immune cells that promote inflammation. These immunce cells release inflammatory molecules that trigger cell death in sperm-producing cells and boost inflammation, the researchers found.-

Improving sperm quality 

The gut microbiota from people living at high altitudes had higher levels of C. symbiosum and succinate than the microbiota of people living at low altitudes. And mice receiving gut microbiota from people living at high altitudes showed higher succinate levels, more inflammatory immune cells in their testes, and reduced sperm quality compared to mice receiving gut microbiota from people living at lower altitudes.

However, removing inflammatory immune cells or reducing succinate levels prevented sperm damage in mice, the researchers found.

The findings reveal a “gut-testis immune axis” and suggest that gut bacteria can indirectly harm sperm through immune signaling, the authors say. The results, they add, “provide insights into the potential targets for improving male sperm quality in [high-altitude] regions.”

Microbiomepost Microbiomepost.com conducted an exclusive interview with Gianfranco Grompone, Chief Scientific Officer at BioGaia GA to discuss the new evidences about oral microbiome.Distributed across distinct niches such as the tongue, palate, dental plaque, and saliva, the oral microbiome comprises more than 700 microbial species, including bacteria and fungi, organized in resilient biofilms. When this ecosystem shifts toward dysbiosis—often characterized by periodontal pathogens—inflammatory conditions can emerge, including gingivitis and periodontitis, and complications may follow dental procedures such as orthodontic interventions or peri-implantitis. Increasingly, research is also linking the oral microbiome to other body sites, particularly the gut, raising the possibility that oral microbial signatures could serve as proxies for broader systemic health. Emerging evidence suggests associations between specific periodontal pathogens and diseases such as type 2 diabetes, neurological disorders, and colorectal cancer, with Fusobacterium nucleatum frequently cited in this context. Within this landscape, clinically supported probiotics are being investigated as a targeted strategy to modulate oral dysbiosis and inflammation. One approach discussed involves a synergistic combination of Lactobacillus reuteri strains (DSM 17938 and ATCC PTA 5289), developed to reduce periodontal pathogen burden while also attenuating inflammatory processes. More than 70 randomized controlled trials across indications—including gingivitis, periodontitis, peri-implantitis, dental plaque, and caries prevention—were referenced, underscoring the growing role of evidence-based probiotics in oral health.

The findings, published in Cell, could help predict and manage microbiota changes after drug treatment.

“Human gut bacteria are routinely exposed to stresses, and community-level responses are difficult to predict,” the authors say. In particular, how antibiotics and other drugs influence complex microbial communities and how interactions among species shape overall community responses is unclear.

The team, led by Handuo Shi at Stanford University in California, used simplified human gut microbial communities—lab-grown mixtures of gut bacteria from a human donor—to study how drugs affect the gut microbiota.

Community responses

The researchers tested how simplified human gut microbial communities respond to 707 different drugs, most of which can be taken orally. They found that many antibiotics reduced community growth, while non-antibiotic drugs had weaker effects. 

Drugs that inhibited growth also changed which species thrived: dominant species were suppressed, allowing rare species to expand. These changes in microbiota composition were linked to how the community consumed nutrients.

Next, the researchers studied how gut bacteria respond to drugs when they are in isolation or when they’re part of a community. While some species were similarly affected in both settings, other species thrived in the community if competitor bacteria were depleted. The effects observed were mostly due to nutrient competition, likely because when dominant species are depleted, the nutrients they normally use become available to other species. 

Predicting drug effects

After drug treatment, gut microbial communities could recover partially or fully, but recovery was more complete when missing species were reseeded, the researchers found.

When communities were treated with drugs multiple times, most species showed similar responses across treatments, while only a small fraction of bacteria, including Flavonifractor plautii, developed resistance. Combining these data with computational models could predict many community-level drug responses. 

Although real gut environments involve additional factors such as interactions with the host, “nutrient competition provides a predictive framework to anticipate and potentially mitigate drug side effects on the gut microbiota,”  the authors say.

Bacteriophages—viruses that infect bacteria—represent a largely underestimated challenge in the manufacturing of fermented foods and probiotic products, particularly when lactic acid bacteria are grown in milk-based matrices. In natural ecosystems, phage–bacteria interactions are highly dynamic, with an estimated 50% of all bacteria being lysed daily as a consequence of viral infection. In industrial settings, however, such infections can severely compromise large-scale production of cheese, yogurt and probiotic preparations by destroying starter or probiotic cultures.

This interview focused on bacteriophages infecting lactic acid bacteria used in food and probiotic applications, addressing three main questions: what these phages are, what they have in common, and how they recognize their specific bacterial hosts. Like many viruses, bacteriophages display a narrow host range, and their ability to discriminate between closely related bacterial strains depends on precise recognition mechanisms. In the case of lactic acid bacteria, current evidence indicates that extracellular polysaccharides act as key receptors, providing the molecular structures that phages bind to in order to attach to, and infect, their preferred hosts.

The second part of the interview explored practical strategies to mitigate phage-related problems. A central concept is the mobilization and exploitation of the inherent immune and defense systems that bacteria have evolved over millions of years of co-existence with viruses. By identifying these naturally occurring anti-phage systems and introducing them into selected industrial or probiotic strains, it is possible to enhance the robustness of starter and probiotic cultures. Such approaches offer a promising route to safeguard the continuous supply of high-quality dairy and probiotic products and to secure the future use of these beneficial bacteria for human health.

The article, published in Trends in Microbiology, describes a 15-year collaboration between researchers led by Raul Tito at KU Leuven in Belgium and the Matsés people of the Peru–Brazil border. The collaboration was rooted in community-based participatory research—an approach that treats Indigenous communities as equal partners rather than subjects of study. 

Like other Indigenous peoples, the Matsés have unique gut microbes that can help advance our understanding of human evolution and improve global health. Gaining this knowledge, however, requires ethical research and strong, trust-based partnerships.

Building partnerships

To establish this collaboration, the researchers first learned about Matsés leadership structures, health concerns, and cultural beliefs. Rather than using standard Western interview techniques, they held open community discussions that fit the Matsés’s way of making decisions. Recognizing the authority of the chief and local delegates was key to build trust among the Matsés, who are historically wary of outsiders.

The researchers learned that concepts such as consent and privacy have different meanings in Matsés culture. Health is seen as a communal right, not an individual issue, and participation in research was often viewed as a collective act of pride. 

The researchers also launched a voluntary screening program for intestinal worms and parasites. Coordinated with local health workers, the program provided medical benefits and opened dialogue about gut health and the human microbiota.

Sharing benefits 

In the guts of Matsés people, the researchers identified new microbial species, including a harmless Treponema strain found in ancestral human populations but largely absent in industrialized societies. This finding may help scientists understand how gut ecosystems evolved and how they influence health. 

Over time, the Matsés participants began to ask questions about the fate of their biological samples and the potential for commercial use. So, the researchers developed a benefit-sharing agreement that guarantees equal profit from any commercialization of microbial discoveries. 

Ethical research with Indigenous communities cannot rely only on external regulations, which are often incomplete or absent in low- and middle-income countries, the authors say. “Establishing genuine partnerships with Indigenous peoples requires sustained investment in trust-building, honest engagement with historical and structural injustices, and a recalibration of scientific practices to prioritize respect, autonomy, and justice,” they say. “Trust must be actively cultivated through shared purpose and mutual accountability.”

The findings, published in Cell Reports Medicine, suggest that extreme longevity arises from the interplay between genetic and environmental factors, offering insights into the mechanisms of healthy aging.

“In Catalonia, the historic nation where M116 lived, the life expectancy for women is 86 years, so she exceeded the average by more than 30 years,” the authors say. Though more people now live past 100, reaching beyond 110 is still extremely rare, and scientists don’t know why people such as M116 achieve such extraordinary longevity.

To uncover some clues, Eloy Santos-Pujol at the Central University of Catalonia in Barcelona, Spain, and his colleagues examined M116’s blood, DNA, metabolism, immune system, microbiota, and epigenetic marks—chemical tags on the DNA that regulate gene expression.

Protective biology

M116’s chromosomes looked normal but her telomeres—the protective caps on DNA that shorten with age—were unusually short. Her genome contained some rare genetic variants that might explain her longevity. These were linked to healthy immune responses, heart function and brain protection.

M116’s mitochondria—the cell’s powerhouses—worked better than those in younger women, and her immune system showed unique characteristics that promoted low inflammation levels. She also had one of the healthiest cholesterol profiles ever recorded, the researchers found.

Although she had some of the typical age-related changes, her cells showed protective epigenetic marks at certain DNA regions, which may have helped prevent disease.

Extreme longevity

M116’s microbiota was unusually diverse and rich in Bifidobacterium—a beneficial gut microbe that usually declines with age. Bifidobacterium has been shown to help fight inflammation and support healthy fats. At the same time, she had few harmful bacteria linked to frailty and inflammation.

The abundance of Bifidobacterium may explain M116’s excellent cholesterol profile and low inflammation levels, the researchers say. Her healthy microbiota, they add, may have been boosted by a Mediterranean diet and daily yogurt, which encourage Bifidobacterium to grow. 

“The picture that emerges from our study, although derived only from this one exceptional individual, shows that extremely advanced age and poor health are not intrinsically linked and that both processes can be distinguished and dissected at the molecular level.”

The study, published in mBio, proposes a coordinated framework involving policymakers, scientists, educators, and communities to embed microbiota science into One Health strategies.

In 2022, global health organizations, including FAO and WHO, launched the One Health Joint Plan of Action (OHJPA) to guide policies, research, and investments to protect people, animals, plants, and the planet. However, although the microbiota is known to play a key role in health and ecosystems, it isn’t mentioned in the plan. 

Estelle Couradeau at the Pennsylvania State University in University Park and her colleagues set out to highlight how microbiota science can help tackle global health problems. They also offered recommendations for making microbiotas a central part of the One Health approach.

Embedding knowledge

A microbiota is a community of microorganisms—including bacteria, fungi and viruses—that lives in humans, animals, plants, soil, water, and air. Microbiotas move between hosts and environments, and understanding how they travel and function could improve disease prevention, environmental protection, and overall health, the researchers say.

The authors propose integrating microbiota science into each of the six OHJPA action plans. For strengthening health systems, they suggest embedding microbiota knowledge into policies, training programs, and governance, while promoting international collaboration and data sharing. For preventing zoonotic diseases, they recommend microbiota-based surveillance to detect early warning signs of disease spillover. For controlling endemic and vector-borne diseases, they propose strategies such as introducing beneficial microbes into vectors, monitoring livestock microbiotas, and encouraging microbiota-friendly farming.

For food safety, the authors advocate for using microbiotas to prevent contamination and improve soil health. To combat antimicrobial resistance, they propose replacing or reducing antibiotic use with beneficial microbes, tracking resistance through microbiota monitoring, and supporting microbiota-based antimicrobial strategies. Finally, for protecting the environment, they recommend leveraging microbiotas for biodiversity conservation, carbon sequestration, waste degradation, and climate resilience.

One Health plan needs clear roles

However, including microbiota science in the One Health plan needs clear roles, the authors say. Governments should set laws and training for microbiota use, while global organizations should create standards and support poorer nations. Professionals across health, agriculture, and environment should apply microbiota solutions, backed by researchers, educators, public campaigns, and the private sector. 

Low- and middle-income countries need capacity building and funding, and global cooperation can help make microbiota science a powerful tool for protecting health, the authors say.

“Taken together, this coordinated, stakeholder-specific approach ensures that microbiome integration is both actionable and transformative across the One Health agenda.”

The findings, published in Cell Host & Microbe, suggest that restoring beneficial bacteria could lead to new treatments for chronic pain in people with sickle cell disease.

Researchers have long suspected that damage from sickled red blood cells may disrupt gut bacteria, and studies show that people with the disorder have different gut bacteria than healthy individuals. However, it’s unclear whether chronic pain in sickle cell disease could be directly driven by gut-related factors.

So, Amanda Brandow at Medical College of Wisconsin in Milwauke and her colleagues set out to investigate how gut bacteria contribute to chronic pain in mice with the disorder.

Pain drivers

Compared to healthy mice, those with sickle cell disease had a different mix of gut bacteria, with lower amounts of Akkermansia muciniphila—a bacterium known to support gut health. When these mice were given gut bacteria from healthy mice, their pain temporarily decreased. Giving the animals A. muciniphila also eased several types of pain. 

Next, the researchers gave healthy mice fecal transplants from either mice with sickle cell disease or healthy animals. The mice that received gut bacteria from diseased animals developed pain symptoms—including sensitivity to cold and heat—while those given gut bacteria from healthy mice did not. 

The pain was linked to increased activity in nerve cells that connect the gut to the brain through the vagus nerve. The researchers also observed that certain chemical byproducts from red blood cell breakdown, such as biliverdin and bilirubin, were much higher in the stool of mice with sickle cell disease than in healthy animals. 

Pain management

Giving healthy mice bilirubin caused pain symptoms and made some nerve cells connected to the gut more excitable, sending stronger signals through the vagus nerve to the brain. Bilirubin activates these gut nerves by binding to specific channels called TRPM2. Blocking these channels with a drug reduced pain in both diseased mice and those given gut bacteria from animals with sickle cell disease. 

People with the condition also have elevated blood bilirubin and fewer bilirubin-processing gut bacteria, the researchers found. This suggests that sickle cell disease patients may have unusually high bilirubin levels, which could overstimulate pain pathways, the authors say.

The findings may pave the way for new therapeutic strategies to help manage chronic pain, they add. “Chemical or probiotic therapies that reduce gastrointestinal bilirubin should be further studied to determine their efficacy in [sickle cell disease] pain management.”

The findings, published in Cell Host & Microbe, could pave the way for targeted therapies such as customized probiotics and diet-based interventions.

Scientists have known that some Bifidobacterium species can live in many hosts, while others are more specialized. But while studies suggest that closely related hosts tend to have similar gut microbes—likely due to co-evolution over time—a detailed understanding of how specific Bifidobacterium strains evolve and function across different hosts is lacking.

Magdalena Kujawska at the University of Birmingham, UK, and her colleagues set out to study Bifidobacterium in 126 animal species across mammals, birds, reptiles, and insects.

Microbial patterns

The researchers analyzed gut microbes from 219 fecal samples and found that different animal groups showed distinct microbial patterns, influenced by evolution and diet. 

For example, mammalian carnivores shared similar gut microbes with birds of prey, and certain primates, including tamarins and marmosets, had particularly high levels of Bifidobacterium.

A closer analysis of 62 mammal and 38 bird species revealed that mammal gut microbes are more influenced by host evolution than bird microbes. The researchers could trace shifts in microbial communities in ancestral species and found patterns tied to diet and lifestyle, with carnivorous mammals and birds having high levels of Clostridiales and Enterobacteriales bacteria, and primates showing increases in Bacteroidales. 

Diverse functions

Bifidobacterium species associated with mammals carry enzymes for breaking down complex sugars, transporting nutrients, and making vitamins, while insect-associated strains focus on simpler sugars needed for energy production, the team found. 

Similarly, primates had the most diverse set of carbohydrate-digesting enzymes, especially those that break down host-derived sugars, and insect-associated strains had the fewest and simplest enzymes.“This research significantly broadens our understanding of the evolutionary biology and functional ecology of Bifidobacterium,” the authors say. “Future research should explore how dietary and ecological components influence microbiota across hosts, enhancing our understanding of gut microbiota dynamics and their functional roles in health and disease.”