The findings, published in Nature Medicine, suggest that the therapy is safe and effective at reducing recurrence of C. difficile infection.

Previous studies using fecal microbiota transplants and microbiota-based therapies suggest that restoring gut bacteria could prevent recurrent C. difficile infection. In particular, VOS—an FDA-approved oral microbiota therapy, made of purified Firmicutes spores from healthy donors—has been shown to reduce infection risk compared to traditional fecal transplants. 

However, it’s unclear which specific bacterial species or metabolites are most important, and how VOS prevents recurrent C. difficile infection at a mechanistic level. So, Jessica Bryant at Seres Therapeutics in Cambridge, Massachusetts, and her colleagues conducted a clinical trial testing VOS in people with recurrent C. difficile infection.

Restoring the microbiota

The researchers gave either VOS bacteria or a placebo to 182 people who had recently taken the antibiotic vancomycin and had at least three C. difficile infection. Stool samples were collected before and after treatment to track how VOS bacteria colonized the gut.

Compared with people receiving the placebo, those who received VOS had more beneficial bacterial species appear in their guts, with more protective Firmicutes and fewer Proteobacteria and other disease-associated species. These bacteria stayed in the participants’ guts for at least 24 weeks, the researchers found.

In contrast, people on the placebo had slower and incomplete microbiota recovery, with fewer beneficial bacteria and more harmful species persisting in their guts. Participants who received VOS did not report significant side effects compared to those receiving the placebo.

Preventing recurrence

Before VOS treatment, participants had high levels of primary bile acids and low levels of protective secondary bile acids, a pattern that favors C. difficile growth. After VOS treatment, secondary bile acids and beneficial fatty acids increased rapidly, while primary bile acids decreased. 

Laboratory tests confirmed that these fatty acids can slow or stop C. difficile growth. Similar changes were also produced by VOS bacterial spores outside the body, suggesting that the treatment restores gut metabolites that help block infection, the authors say.“These data support a potential role for VOS, after antibiotic therapy, to restore the microbe-associated metabolic functions needed to prevent [C. difficile infection] recurrence.”

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 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 Cell Host & Microbe, suggest that these bacteria must be used with caution in probiotics and microbiota-based therapies.

Before this study, not much was known about whether lantibiotic-producing bacteria influence the recolonization of the gut microbiota, how they impact beneficial bacteria, and whether interventions such as fecal transplants could restore microbiota diversity in their presence.

So, Cody Cole at the University of Chicago in Illinois and his colleagues studied how a lantibiotic-producing gut bacterium called BpSCSK affects gut recovery after antibiotic treatment.

Dominating the microbiota

In mice with a full gut microbiota, BpSCSK could not establish itself in the intestine. However, after antibiotics, which reduced resident bacteria, BpSCSK successfully colonized the gut and became the dominant species. 

BpSCSK also prevented gut bacteria, including those that produce beneficial compounds such as short-chain fatty acids, from returning. For weeks after colonization with BpSCSK, mice had lower gut bacterial diversity and decreased levels of beneficial metabolites such as butyrate. 

Even when the researchers tried to restore the gut microbiota with a fecal transplant from healthy mice, BpSCSK continued to be dominant, preventing many other bacteria from colonizing the gut. 

Infection susceptibility

Mice colonized with BpSCSK after antibiotics became more vulnerable to infections with opportunistic pathogens such as Klebsiella pneumoniae and Clostridioides difficile, showing weight loss and metabolic changes that favor pathogen growth. 

However, when the animals were exposed to a microbiota that had previously developed with BpSCSK, this community of bacteria successfully colonized the gut, reducing BpSCSK’s dominance. In these mice, microbial diversity was restored and the levels of beneficial metabolites grew, the researchers found.

The findings suggest that lantibiotic-producing bacteria can have a detrimental role in microbiota diversity and function, the authors say. “More work is needed to determine the therapeutic potential of lantibiotics and to better characterize the novel lantibiotics currently found in probiotics and microbiomes to mitigate off-target side effects that could impair commensal bacterial functions.”

At birth, contact with maternal and environmental microbes initiates a rapid colonisation of the neonatal gut. This early community, enriched in obligate anaerobes such as bifidobacteria, interacts with pattern-recognition receptors on epithelial and immune cells (for example Toll-like receptors and NOD-like receptors), promoting the maturation of gut-associated lymphoid tissue and the establishment of oral tolerance. When this process is perturbed, for instance by caesarean delivery or antibiotics, experimental and human data suggest an increased risk of allergy, autoimmunity and infection later in life. [1]

Microbial metabolites as key mediators of gut–immune communication

Microbial metabolites are central to this immune dialogue. Short-chain fatty acids (SCFAs) such as acetate, propionate and butyrate, produced by the fermentation of dietary fibres, act as signalling molecules that influence T-cell differentiation, B-cell antibody production and epithelial barrier integrity. Butyrate, in particular, promotes the differentiation of colonic Foxp3⁺ regulatory T cells via histone deacetylase inhibition and G-protein-coupled receptor signalling, thereby dampening excessive inflammation and protecting from colitis in preclinical models. [2] More recent work confirms that SCFAs can drive both effector and regulatory responses, with the net effect depending on tissue context and inflammatory tone, and that SCFA-mediated imprinting of T cells is a promising therapeutic lever in immune-mediated disease. [3]

When the composition or function of the gut microbiome is disturbed, so-called dysbiosis, the result can be a breakdown of immune homeostasis. Inflammatory bowel disease (IBD), for example, is characterised by reduced microbial diversity, depletion of SCFA-producing taxa and expansion of pathobionts, all of which correlate with impaired barrier function and exaggerated mucosal immune responses. [4] Similar patterns are increasingly described in systemic conditions such as rheumatoid arthritis (RA), where specific microbial signatures and metabolite profiles associate with autoantibody formation and disease activity, suggesting that gut dysbiosis may contribute causally to the loss of tolerance. [5] More broadly, the gut microbiota is now viewed as a druggable target in immune tolerance and autoimmunity, with strategies ranging from diet and prebiotics to defined consortia of “immunobiotics”. [6]

Within this conceptual framework, strain-selected probiotics, particularly bifidobacteria and lactobacilli sensu lato, are being evaluated as tools to reinforce mucosal defences and re-establish balanced immune responses. Preclinical models show that certain Bifidobacterium breve strains can attenuate allergic inflammation by enhancing regulatory T-cell activity and skewing T-helper responses away from Th2 dominance, while also modulating gut microbiota composition.  [7] Other B. breve strains improve immune function in immunosuppressed animals, for example by restoring splenic and intestinal cytokine profiles and reducing oxidative stress. [8] In parallel, clinical and translational data for Lactobacillus/Lacticaseibacillus and related species indicate that specific strains can enhance vaccine responses, support upper respiratory tract defences and reduce the incidence or duration of respiratory infections, especially in children. [9]

Coree infant-derived probiotic strains as tools to reinforce mucosal immunity

Three infant-derived strains, Bifidobacterium breve 2TA LMG P-30999, Lactobacillus gasseri L6 LMG P-30998 and Lacticaseibacillus rhamnosus (formerly Lactobacillus rhamnosus) L13b LMG P-31000, isolated and developed by Coree srl are potentially interesting for immune support. These strains have been genomically characterised for safety (absence of acquired antibiotic-resistance and virulence genes) and equipped with traits relevant for gut survival, such as acid and bile tolerance and adhesion factors, supporting their use as next-generation probiotics. 

B. breve LMG P-30999, isolated from infant faeces, combines classical bifidobacterial features, such as the ability to utilise human milk oligosaccharides and synthesise B-group vitamins, with a strong immunomodulatory profile. In the Coree in-vitro platform, this strain induces IL-10 release from human peripheral blood mononuclear cells, consistent with a tolerogenic, anti-inflammatory imprinting of host immunity, and contributes to down-regulation of pro-inflammatory cytokines (TNF-α, IL-8) in inflamed intestinal epithelial cells, particularly in a preventive (pre-treatment) setting. [10] These observations mirror the broader literature in which B. breve strains alleviate experimental allergic rhinitis and food allergy by expanding CD4⁺CD25⁺Foxp3⁺ regulatory T cells and normalising Th1/Th2 balance, as well as improving immune status in chemically immunosuppressed mice. [7] From a translational perspective, LMG P-30999 thus appears particularly attractive for early-life formulations aimed at supporting physiological immune maturation and promoting tolerance in at-risk populations, pending dedicated clinical trials.

L. gasseri LMG P-30998, also infant-derived, carries genes for acid and bile resistance and encodes bacteriocin production, suggesting a capacity to both persist in the gut and inhibit competing pathobionts. In Coree’s human cell models, viable and heat-inactivated preparations of this strain stimulate IL-10 and, notably, IL-12p70 in peripheral blood mononuclear cells, a cytokine profile compatible with balanced activation of innate and Th1-type responses without excessive inflammation. [10] This fact fits well with data from other L. gasseri / L. paragasseri strains, where oral intake has been shown to increase mucosal secretory IgA, enhance influenza vaccine-specific antibody responses, and reduce common cold symptoms while modulating NK-cell and innate immune markers in healthy adults. [9] Combined with the dossier’s demonstration of antioxidant properties and capacity to attenuate cytokine responses in inflammatory models, LMG P-30998 emerges as a promising candidate to reinforce mucosal barrier and humoral defences in the upper and lower airways as well as in the gut, potentially also in heat-inactivated (postbiotic) formats. 

Lacticaseibacillus rhamnosus LMG P-31000 stands out for a particularly broad range of immune-relevant activities. In Coree’s in-vitro systems, this strain induces IL-10 in human immune cells, mitigates IL-6 and IL-8 up-regulation in epithelial models exposed to chemical or pathogen-induced inflammation, and displays anti-biofilm activity against key respiratory and skin pathogens when used as a postbiotic. It also counteracts oxidative stress in Caco-2 cells and helps maintain tight-junction gene expression after hydrogen peroxide exposure, pointing to a role in preserving barrier integrity under inflammatory conditions. Remarkably, LMG P-31000 reduces PD-L1 expression in colorectal cancer cell lines and shows additive effects with a PD-L1 inhibitor, suggesting a potential adjuvant role in checkpoint blockade therapy, though this remains entirely preclinical at present. [10]

These properties are highly consistent with the extensive literature on L. rhamnosus GG (LGG) and related strains. Randomised controlled trials and meta-analyses have reported reductions in upper respiratory tract infections, acute otitis media and antibiotic use in children receiving LGG, as well as shorter duration of respiratory symptoms in specific subgroups. [11] Although strain-specificity is crucial and the Coree LMG P-31000 strain requires its own clinical documentation, its in-vitro signature—combining immunomodulation, barrier protection and anti-biofilm activity—aligns with the immunobiotic profile that has made L. rhamnosus species a cornerstone of probiotic research.

From microbiome–immune crosstalk to strain-level interventions and future perspectives

Taken together, the available evidence underscores a continuum from ecosystem-level microbiome–immune crosstalk to strain-level interventions. A healthy, fibre-fed gut microbiome provides a metabolite environment that supports regulatory T-cell differentiation, robust barrier function and effective, but not excessive, immune responses. [2] Within this framework, strains such as B. breve LMG P-30999, L. gasseri LMG P-30998 and L. rhamnosus LMG P-31000 represent rationally selected tools to reinforce specific facets of mucosal immunity, tolerance, humoral protection and barrier integrity, while also offering postbiotic applications where the use of viable bacteria is not desirable. The next step will be to translate their promising preclinical profiles into well-designed human trials that define indications, target populations and clinically meaningful immune outcomes.

References

PubMed-indexed sources, in order of citation

1. Yoo JY, Groer M, Dutra SVO, Sarkar A, McSkimming DI. Gut microbiota and immune system interactions. Microorganisms. 2020;8(10):1587. PMID: 33076307. 
2. Furusawa Y, Obata Y, Fukuda S, et al. Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells. Nature. 2013;504(7480):446–450. PMID: 24226770. 
3. Saadh MJ, Aldossary AM, Al-Harthi J, et al. The effects of microbiota-derived short-chain fatty acids on T-cell function. Semin Immunol. 2025;69:101812. PMID: 40136436.
4. Bretto E, Urpì-Ferreruela M, Casanova GR, González-Suárez B. The Role of Gut Microbiota in Gastrointestinal Immune Homeostasis and Inflammation: Implications for Inflammatory Bowel Disease. Biomedicines. 2025 Jul 24;13(8):1807. doi: 10.3390/biomedicines13081807. PMID: 40868062; PMCID: PMC12383986.
5. Qi P, Chen X, Tian J, Zhong K, Qi Z, Li M, Xie X. The gut homeostasis-immune system axis: novel insights into rheumatoid arthritis pathogenesis and treatment. Front Immunol. 2024 Sep 26;15:1482214. doi: 10.3389/fimmu.2024.1482214. PMID: 39391302; PMCID: PMC11464316.
6. Almansour N, Howell N, Candon S. Gut microbiota: a promising new target in immune tolerance. Curr Opin Immunol. 2025;87:102349. PMID: 40084744.
7. Ren J, Liu T, Liu X, et al. Effects of Bifidobacterium breve feeding strategy and delivery modes on allergic rhinitis in mice. PLoS One. 2015;10(10):e0140018. PMID: 26439865.
8. Fang H, Chen X, Lu W, et al. Bifidobacterium breve CCFM1310 enhances immunity in cyclophosphamide-induced immunosuppressed mice. J Funct Foods. 2024;115:105071. PMID: 38747771.
9. Nishihira J, Kagami-Katsuyama H, Tanaka A, et al. Lactobacillus gasseri SBT2055 stimulates immunoglobulin production and innate immunity after influenza vaccination: a randomized double-blind, placebo-controlled trial. Funct Foods Health Dis. 2016;6(9):544–568. PMID: 28491071.
10. Internal data, available upon request
11. Hojsak I, Snovak N, Abdović S, et al. Lactobacillus GG in the prevention of gastrointestinal and respiratory tract infections in children attending day care centers: a randomized, double-blind, placebo-controlled trial. Clin Nutr. 2010;29(3):312–316. PMID: 19896252.

In this interview, the microbiologist retraces a 20-year research journey at INRAE, France’s public institute for agriculture, food and environment, where his laboratory investigates interactions between probiotics, commensal bacteria and the host, with a focus on inflammation and inflammatory bowel diseases (IBD). 

The turning point came with clinical observations in Crohn’s disease: together with gastroenterologist Harry Sokol, Langella compared the gut microbiota of patients in relapse versus remission and found that those in relapse had markedly reduced levels of Faecalibacterium prausnitzii, while patients in remission showed higher abundances. This led to the hypothesis that F. prausnitzii could be a beneficial commensal. Subsequent work, published in 2008, demonstrated in murine models of chemically induced colitis that both the live bacterium and its culture supernatant could ameliorate inflammation and restore gut health. Mechanistic studies identified butyrate production and, crucially, a secreted protein termed MAM (microbial anti-inflammatory molecule), which exhibits strong anti-inflammatory activity and whose efficacy varies across F. prausnitzii strains. 

In 2016, this body of work gave rise to the startup Exeliom Biosciences, co-founded by Langella and partners from gastroenterology, industrial fermentation and biotech. The company has industrialized a drug product, strain EXL01, and shown in mouse models that it can counteract Clostridioides difficile infection and enhance responses to immune checkpoint inhibitors by modulating the gut microbiota. EXL01 is now being evaluated in multiple human clinical trials in cancer, IBD and C. difficile infection, with a phase 1 study in IBD (“MAINTAIN”) completed without safety issues, marking a key step in translating a commensal bacterium into a next-generation microbiome-based therapy.

The findings, published in Cell, highlight the importance of understanding skin microbiotas to manage long-term fungal infections in Indigenous communities—work that may help develop better diagnostics and treatments.

Unlike the gut microbiota, the skin microbiota is poorly understood, especially in non-urbanized populations, and only a few studies have focused on Indigenous groups.

For example, Malaysia’s Indigenous Orang Asli community suffers from a chronic fungal disease that causes scaly skin rashes. Treatment is challenging because of limited access to the community, which has a semi-nomadic lifestyle. 

From 2022 to 2023, researchers led by Yi Xian Er at Malaya University in Kuala Lumpur, Malaysia, studied 82 people from the Orang Asli community, 20 of whom were infected with the fungus Trichophyton concentricum, which causes a chronic fungal disease called tinea imbricata.

Drug resistance

Although the study participants came from five villages up to 440 km apart, their fungal strains were genetically similar, which indicates that the infection is not from a single source. Some genetic similarities were found within families or between nearby villages, hinting at shared exposure or past transmission. 

The researchers tested 60 T. concentricum samples from the Orang Asli community against eight common antifungal drugs. Most drugs worked well, but some were less effective. About 15% of the samples—mainly from two people in one village—showed signs of resistance to terbinafine, a commonly used drug, due to a genetic mutation that has also been found in resistant cases worldwide. 

The team also compared the skin microbiotas of Orang Asli and people from urban areas in Malaysia and the United States. Orang Asli’s skin microbes were not well represented in existing databases, so the researchers created new genetic profiles of bacteria and fungi from this population, which may help to improve future studies of skin conditions such as tinea imbricata.

Diverse microbiota

The skin microbes of Orang Asli individuals were more diverse than those of people living in urban areas such as Kuala Lumpur and Washington, DC, the researchers found. 

Orang Asli had high levels of certain bacteria not commonly found in cities, while urban populations had high amounts of common skin bacteria such as Cutibacterium acnes, Corynebacterium tuberculostearicum, and Staphylococcus epidermidis. These differences were linked to lifestyle factors such as sanitation, diet, and contact with nature. People with tinea imbricata had much higher levels of T. concentricum on their skin compared to healthy people, who showed no signs of the fungus.

“These findings provide valuable insights into clinical, microbiological, and genomic features of chronic fungal skin infections, offering the potential to inform strategies to address drug resistance and effective therapy,” the authors say.

The findings, published in Cell Host & Microbe, indicate that a healthy, diverse gut microbiota is important for mounting strong and lasting immune responses to vaccination.

The results, the authors say, “have broader implications for personalized vaccine strategies and public health implications, antibiotic stewardship and vaccine policy, the role of the microbiome in vaccine development, and therapeutic interventions to enhance immune responses to vaccines.”

Previous studies have shown that a protein called TLR5, which detects bacterial components in the gut, helps boost antibody production after vaccination. However, direct proof of the microbiota’s impact on immunity remains limited. 

So, researchers led by Yupeng Feng at Stanford University in California set out to examine how broad-spectrum antibiotics, which disrupt the gut microbiota, affect the immune response to a new vaccine in people.

Supporting immunity

In the study, 18 people received two doses of the rabies vaccine—one on day 0 and another on day 28. Half of them took antibiotics for 5 days after the first vaccine dose, while the other half did not take antibiotics.

Antibiotics lowered the number of gut bacteria by more than 100 times and changed the microbiota composition, with certain bacteria becoming temporarily dominant. Although microbial levels gradually returned to normal in people who took antibiotics, bacterial diversity stayed low for months. 

People who took antibiotics had an antibody response nearly six times lower than that of the control group, and this weaker response lasted up to six months. They also had lower levels of protective antibodies and fewer active immune cells that usually help fight off infections. 

Increased inflammation

Compared to the control group, participants who took antibiotics showed stronger and longer-lasting signs of inflammation. Analyses of blood samples revealed that antibiotics combined with the vaccine caused changes in metabolites, including increases in certain fat-related compounds and decreases in others. 

Antibiotics also lowered the levels of secondary bile acids, which are made by gut bacteria and help regulate inflammation. Overall, the authors say, antibiotics disrupted the body’s metabolic balance, which may in turn affect immune responses.

The findings, they add, suggest that a healthy gut microbiota is important in supporting effective immune responses to vaccines by regulating inflammation, metabolism, and immune cell behavior.

The findings, published in mBio, highlight the potential for dietary interventions in treating C. difficile infection and inflammatory conditions such as inflammatory bowel disease.

Previous research has shown that diet can modulate the microbiota and influence the severity of C. difficile infections. For example, certain foods, such as fiber, seem to reduce disease severity, while high-fat and high-protein diets may worsen it. 

Studies in mice have shown that different standard lab diets can affect C. difficile infection severity. However, even when using the same type of mice and treatment protocol, disease severity varied between different research facilities. The key difference was the type of standard mouse chow used: mice fed Diet 5010 experienced severe illness, while those on Diet 5053 had milder symptoms.

To better understand the link between diet and disease severity, Joshua Denny at the University of Pennsylvania in Philadelphia and his colleagues set out to compare Diet 5010 and Diet 5053.

Protective effect

Despite having similar levels of C. difficile in their guts, mice fed Diet 5053 showed less intestinal damage and inflammation than those fed Diet 5010. Mice fed Diet 5053 also had a more controlled immune response with reduced inflammation and tissue damage compared to those on Diet 5010.

Even after antibiotic treatment, mice on Diet 5053 had more beneficial gut bacteria such as Lactobacillaceae than mice on Diet 5010, the researchers found.

Further analyses revealed differences in gut metabolites between mice: those fed Diet 5053 had high levels of flavonoids, which are known for their anti-inflammatory effects. This unique metabolite signature suggests that Diet 5053 helps limit inflammation, the researchers say. 

Anti-inflammatory metabolites

When tested in a mouse model of colitis, Diet 5053 reduced disease severity and weight loss compared to Diet 5010, the researchers found. 

To explore the role of gut bacteria in protecting against infection, the team compared the diets in mice from different breeding facilities, which are known to have distinct microbiota compositions. Diet 5053 provided better protection against infection and colitis, but only in mice with a diverse microbiota. 
The findings suggest that the protective effects of Diet 5053 depend on the microbiota’s production of anti-inflammatory metabolites, which help reduce inflammation and maintain the intestinal barrier against C. difficile infection and colitis, the authors say. However, they add, “more research is needed to understand the mechanistic role of Diet 5053 and how these findings may apply more specifically to C. difficile infection and [inflammatory bowel disease] in humans.”