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.”

The findings, published in Science Immunology, suggest that leveraging gut-lung interactions could offer new ways to prevent or reduce severe complications from respiratory viral infections.

One reason people get secondary infections after flu is that the virus damages lung immune cells called alveolar macrophages (AMs). SFB can help AMs stay strong during viral infections, but it’s unknown whether these microbes protect against secondary infections and how they might do so.

Researchers led by Vu Ngo at Georgia State University in Atlanta studied whether SFB protect mice from deadly bacterial infections after flu.

Boosting immunity

The team compared mice with and without SFB in their gut. Animals without SFB lost a lot of AMs and had severe lung infections after flu. In contrast, mice with SFB had strong AMs and showed much less lung damage and fewer bacteria. But when the researchers removed AM cells, even mice with SFB became vulnerable. 

Scientists have known that mice typically acquire SFB from their mothers. Compared to pups of mice without SFB, those of mice with SFB had healthier lungs, fewer bacteria, and better survival after flu and bacterial exposure, and this protection lasted for at least four generations. 

Further experiments showed that SFB work by reprogramming the lung’s AMs to resist flu-induced damage and remain effective at killing bacteria, rather than by bringing new immune cells into the lungs. The microbes also boost antibacterial activity in immune cells throughout the body.

Transferring protection

Next, the researchers found that AMs from mice without SFB lost function in an inflamed environment, but if they were placed in the lungs of mice with SFB, they regained their antibacterial activity. 

Rather than acting only by reducing harmful inflammatory signals, SFB change AMs at the genetic and metabolic level, boosting their ability to kill bacteria, produce immune helpers, and maintain energy. Transplanting AMs from SFB-colonized mice into mice without SFB transferred protection, the researchers found.

“We speculate that defining and subsequently harnessing the mechanism by which SFB colonization reprograms AM will lead to new strategies to mitigate the [respiratory viral infection] induced disease burden,” the authors say.

The findings, published in Nature Communications, suggest that gut microbiota profiles can help support personalized dietary interventions.

Lifestyle changes such as diet and exercise can help people with prediabetes, but individual responses vary due to differences in genetics and gut bacteria. The gut microbiota plays a key role in breaking down dietary fiber to improve insulin activity. However, whether microbial features can predict individual response remains unclear. 

Researchers led by Delei Song at Shanghai Jiao Tong University in China enrolled more than 800 people with prediabetes in a clinical study to investigate whether, and how, dietary fiber supplements can help improve blood sugar control.

Prediabetes subgroups

Study participants were randomly assigned to receive standard care with or without fiber supplements. Researchers grouped participants using multiple health measures, including age, weight, and blood sugar, rather than just blood sugar, and analyzed their gut microbiota. 

This approach identified four subgroups of people with prediabetes, each with distinct health profiles, such as differences in insulin production, heart and liver health, and family history of diabetes. These subgroups also showed differences in gut bacteria and blood metabolites, with some having less diverse gut microbiotas.

Only two of these subgroups benefited from dietary fiber, and this improvement depended on whether their gut bacteria could respond to fiber, the researchers found. 

Personalized medicine 

To predict who would benefit from dietary fiber, they researchers created a score based on changes in three key blood sugar measures. Then, they used machine learning to link these outcomes to specific gut bacteria. A set of specific gut bacteria could predict with good accuracy whether a person would respond well to fiber, the team found. 

Next, the researchers tested this approach in two independent groups of people with type 2 diabetes, showing it could predict both short-term and long-term benefits.

“Our study suggests that the gut microbiota response influences the effectiveness of dietary fiber intervention and provides a clinically applicable model to guide microbiome-targeted personalized medicine for prediabetes,” the authors say.

The findings, published in Science Immunology, suggest that gut Clostridia can be divided into two groups, with one group contributing to gut inflammation under certain conditions.

Scientists have known that Clostridia bacteria make proteins called flagellins, which build flagella. Flagellins can also interact with the immune system, with some triggering only weak immune responses and others causing inflammation. However, it’s unclear how differences in flagellin types affect their ability to stimulate the immune system and which flagellins promote or prevent inflammation in the gut.

To address this question, Lennard Duck at the University of Alabama at Birmingham and his colleagues set out to study more than 100,000 bacterial genomes from gut Clostridia.

Immune activation

The researchers found that the genes controlling flagella, called motility genes, are arranged differently across Clostridia bacteria, even among closely related families. Some bacteria, such as Lachnospiraceae, have multiple motility genes and more diverse flagellins, while others have fewer of these genes and less diversity. 

Based on flagellin diversity and motility gene organization, the team classified gut Clostridia into two groups, G1 and G2. Next, they tested these two groups of bacteria in germ-free mice to see how they affect the gut. 

Both groups could colonize the gut, boost protective immune cells, and stimulate the production of antibodies that help maintain normal gut balance. However, G2 bacteria triggered stronger responses in gut cells, including genes linked to inflammation and stress, while G1 bacteria mainly activated protective functions. 

Gut inflammation 

When the gut’s barrier was weakened, G2 bacteria—but not G1 bacteria—caused inflammation and tissue damage in the colon lining. The researchers found that flagellins differ between G1 and G2 gut bacteria: Most G1 bacteria produce flagellins at very low levels, while G2 bacteria produce flagellins that strongly activate the immune system. What’s more, G2 flagellins stimulate inflammatory signals, whereas G1 flagellins don’t. 

In people with Crohn’s disease, G1 bacteria are typically reduced, while G2 bacteria are more abundant in inflamed tissues, the researchers also found. This finding, they say, suggests that the balance between G1 and G2 bacteria and their flagellins may influence gut inflammation and disease. 

“This study identified key features of specific commensal bacteria that have colitogenic potential and revealed one mechanism whereby these organisms can potentially initiate intestinal inflammation,” the authors say.

The findings, published in Cell Host & Microbe, suggest that the composition of the lung microbiota is shaped by different factors and can influence pneumonia progression and treatment outcomes.

Scientists have known that pneumonia involves changes in the lung microbiota and is often associated with microbial imbalance rather than a single pathogen. However, how distinct lung microbiota “states” form, how stable they are over time, and how they relate to treatment outcomes is unclear.

To address this question, Jack Sumner at Northwestern University in Evanston, Illinois, and his colleagues analyzed the lung microbiota in critically ill patients with and without pneumonia.

Microbial fingerprint

Between 2018 and 2020, the researchers followed 248 people on breathing machines who were suspected of having pneumonia, collecting fluid samples from their lungs to study infections in detail. Doctors classified their conditions into community-acquired, hospital-acquired, or ventilator-associated pneumonia, and most cases were caused by bacteria. 

By analyzing the patients’ lung microbiota, the researchers found that the type of pneumonia was linked to differences in which microbes were present in the lungs and how the patient’s immune cells behaved. 

Pneumonia was linked to shifts in certain bacteria and microbial genes, including lower levels of some normally present microbes and higher levels of others, especially Staphylococcus species, which are often linked to infection and antibiotic resistance. About 36 to 46% of pneumonia samples had disrupted lung microbiotas.

Treatment outcomes

The researchers also found that critically ill patients tend to have a lung microbiota that fall into four main groups, or “pneumotypes”: skin-like, mixed, Staphylococcus-dominated, and oral-like. Each pneumotype had distinct levels of diversity, dominant bacteria, and traits such as antibiotic resistance. 

Oral-like and Staphylococcus-dominated pneumotypes had the highest bacterial levels and greatest immune activation, while skin-like pneumotypes showed the lowest disruption. The oral-like pneumotype was associated with successful pneumonia treatment and recovery, while the skin-like pneumotype was linked to worse outcomes.

“We show that host and microbiota landscapes change in unison with clinical phenotypes and that microbiota state dynamics reflect pneumonia progression,” the authors say. “We suggest that distinct pathways of lung microbial community succession mediate pneumonia progression.”

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 Nature Communications, suggest that rectal mucus sampling is a minimally invasive, effective approach for detecting colorectal cancer and other bowel diseases.

Colorectal cancer involves genetic mutations, changes in chemical tags on the DNA molecule, and alterations in the gut microbiota. These factors can sometimes be detected in tumors, blood, or stool, but it’s unclear whether rectal mucus could serve as a reliable source of disease information.

Andrew Tock at Origin Sciences in Cambridge, United Kingdom, and his colleagues set out to test a device that collects rectal mucus to see if it could help detect colorectal cancer and precancerous lesions.

Combined approach

The researchers analyzed samples from 800 people suspected of colorectal cancer and found that genes such as APC, BRAF, and TP53 were most frequently mutated in those with cancer. The amount of detectable mutations was strongest in cancers located near the rectum, where the sample was collected, than in tumors farther away. 

Many colorectal cancer-related genes were located in DNA regions that had extra chemical tags called methyl groups, especially near key regulatory regions. This “hypermethylation” was most common in rectum cancers. 

The team also identified 36 bacterial species—particularly Hungatella hathewayi and Intestinimonas butyriciproducens—associated with colorectal cancer. Other bacteria, such as Porphyromonas asaccharolytica and Clostridium scindens, also showed associations with cancer. 

Cancer biomarker

Next, the researchers combined the three types of biological data—gene mutations, chemical tags on the DNA, and gut microbiota profiles—obtained from rectal mucus to create a “biomarker” of colorectal cancer. Key mutated genes, hypermethylated DNA regions, and certain bacteria such as Hungatella hathewayi could distinguish cancer cases from healthy controls. 

Precancerous lesions fell between controls and cancers, reflecting their potential to progress to malignancy, and rectal cancers were easier to detect than tumors farther away. 

Larger studies are needed to confirm how well this mucus-based method performs in real-world clinical settings, the authors say. However, they add, “we demonstrate the clinical utility of rectal mucus sampling combined with hologenomic analysis as a translatable prospective tool for diagnostic application.”

The findings, published in Cell Host & Microbe, suggest that targeted dietary strategies could be used to reduce susceptibility to cholera.

Studies have shown that diet influences the gut microbiota and some milk-derived proteins can inhibit cholera toxin activity. However, how specific dietary components affect V. cholerae metabolism and virulence, as well as its interactions with commensal gut bacteria, remains unclear.

Researchers led by Rui Liu at the University of California, Riverside used adult mice to test how different diets affect V. cholerae infection.

Protective diets

The researchers fed mice diets high in carbohydrate, fat, or protein, including protein from casein, soy, or wheat, and then infected the animals with V. cholerae after reducing the mice’s gut microbiota with antibiotics. 

Mice on high-protein diets with casein or wheat protein had much lower levels of V. cholerae colonization compared with mice on high-carbohydrate, high-fat, or soy-protein diets.

V. cholerae in mice fed casein or wheat protein appeared to alter the activity of many genes, reducing some involved in metabolism and virulence. Diets with soy protein did not trigger these changes.

Diet-driven outcomes 

Further experiments revealed that one V. cholerae’s gene, called flrA, is linked to diet-induced changes in metabolism, virulence, and a molecular “weapon” that V. cholerae uses to compete with gut microbes.

Disabling flrA restored bacterial growth and the ability of the bacterium to compete with the resident microbiota, the researchers found.The findings highlight how diet and microbial interactions together may influence the outcome of V. cholerae infection. However, the authors say, “the complexity of actual human diets and microbiota means that the range of potential diet-driven outcomes of V. cholerae colonization or infection is vast and will require much additional study to fully elucidate.”

The findings, published in iScience, suggest that the microbiota could be one of the ways through which owning a dog supports adolescents’ social development and mental well-being.

“Raising dogs has beneficial effects, especially for adolescents, and these effects may be mediated through symbiosis with microorganisms,” says study co-author Takefumi Kikusui at Azabu University in Japan.

Studies have suggested that living with a dog can change a person’s gut bacteria, but it is unknown whether the microbes acquired from living with dogs could affect adolescents’ social behavior or mental well-being. So, Kikusui and his team studied 343 adolescents, some of whom owned a dog, and assessed their microbiota and mental health.

Bacterial differences

Teens who owned a dog at age 13 showed better mental and behavioral health at age 14 than those who did not: they had fewer social problems and less social withdrawal, even after accounting for factors such as family income and size. 

When the researchers analyzed saliva samples from the teens, they found that while overall oral bacteria diversity was similar between groups, certain bacteria were more common in dog owners. 

Some of these bacteria, particularly in Streptococcus strains, were linked to fewer behavioral and attention problems, the researchers found.

Promoting well-being 

To explore whether bacteria from dog-owners could influence social behavior, the researchers transferred saliva microbes from these teens into germ-free mice. 

Compared with mice receiving microbes from teens who didn’t own a dog, those receiving microbes from dog-owning teens showed increased sociability, approaching unfamiliar mice more often. However, these mice also showed more avoidance of new objects. Specific Streptococcus strains were linked to increased sociability in mice, the researchers found.

“The most interesting finding from this study is that bacteria promoting prosociality, or empathy, were discovered in the microbiomes of adolescent children who keep dogs,” Kikusui says. “The implication is that the benefits of dog ownership include providing a sense of security through interaction, but I believe it also holds value in its potential to alter the symbiotic microbial community.”