Oral bacteria play a role in chronic liver disease

The findings of the team led by Prof. Melanie Schirmer provide starting points for new therapies for advanced chronic liver disease.
Photo Credit: Astrid Eckert / TUM 

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Specific oral bacteria were found to translocate to and colonize the gut in patients with chronic liver disease, where they actively contribute to disease progression rather than acting as passive bystanders.
• Mechanism of Action: These translocated bacteria express genes encoding collagen-degradation enzymes (collagenases) that damage the intestinal barrier, allowing bacterial pathogens to leak into the liver and exacerbate fibrosis.
• Methodology: The study combined comparative microbiome sequencing of patient samples with in vivo mouse experiments, demonstrating that introducing these specific oral strains into mice directly worsened gut barrier damage and liver condition.
• Key Observation: While healthy individuals maintain distinct oral and gut microbiomes, patients with advanced liver disease exhibited nearly identical bacterial strains in both sites, indicating significant bacterial migration.
• Diagnostic Application: The presence and abundance of the specific gene responsible for collagen degradation in stool samples were identified as a reliable biomarker for distinguishing patients with liver disease from healthy individuals.
• Therapeutic Potential: These findings suggest that therapies targeting the oral microbiome or inhibiting microbial collagenase activity could restore gut barrier integrity and slow the progression of chronic liver disease.

Not only toxic but also a nutrient: guanidine as a nitrogen source

Cyanobacteria convert light energy into chemical energy through photosynthesis and are becoming increasingly important for carbon-neutral biotechnology.
Photo Credit: André Künzelmann / UFZ

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Cyanobacteria possess the capability to actively absorb and catabolize guanidine (CH5N3) as their sole nitrogen source, refuting the prior scientific consensus that the compound acts exclusively as a toxic denaturant in these organisms.
• Methodology: The study utilized an interdisciplinary approach combining genome analysis, molecular microbiology, biochemical binding assays, and simulation-based process analytics to map the complete metabolic pathway and regulatory networks.
• Specific Mechanism: Uptake is facilitated by a newly identified, high-affinity ATP-binding cassette (ABC) transport system effective at low concentrations, while intracellular guanidine hydrolase converts the substrate into ammonium and urea for metabolic integration.
• Key Regulation Detail: Gene expression for the transporter and hydrolase is controlled by a specific riboswitch that directly binds guanidine, functioning as a precise sensor to regulate uptake and trigger efflux systems if intracellular levels become toxic.
• Ecological Context: These findings suggest that free guanidine is naturally available and constitutes an overlooked but integral component of global biogeochemical nitrogen cycles, providing a colonization advantage for cyanobacteria.
• Future Application: The identified riboswitch mechanism offers a novel, cost-effective molecular tool for synthetic biology, enabling researchers to finely tune gene expression in cyanobacterial "green cell factories" by modulating guanidine levels.

Researcher contributes to study revealing hidden diversity of E. coli in diabetic foot infections

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Escherichia coli found in diabetic foot infections is not a uniform pathogen but constitutes a highly diverse array of genetic groups, with distinct lineages independently adapting to the diabetic wound environment.
• Methodology: Researchers conducted the first comprehensive whole-genome sequencing analysis of 42 E. coli strains isolated from diabetic foot ulcers across diverse global populations, including the UK, Nigeria, Brazil, and the USA.
• Key Statistic: Approximately 8% of the analyzed strains were classified as multidrug-resistant or extensively drug-resistant, possessing mechanisms to withstand multiple or nearly all available antibiotic classes.
• Specific Mechanism: The genomic data identified critical virulence factors—specifically genes enabling tissue attachment and immune evasion—that explain the rapid progression and severity of these infections.
• Significance: This genomic characterization provides a foundation for developing precision diagnostics and targeted therapies, directly addressing the urgent need to reduce treatment failure and lower-limb amputations in diabetic patients.

Plastic particles increase inflammation and cross barriers

Lukas Kenner, visiting professor, Department of Molecular Biology.
Photo Credit: Medizinische Universität Wien

Scientific Frontline: "At a Glance" Summary

• Core Discovery: Micro- and nanoplastics (MNPs) exacerbate chronic inflammatory bowel diseases (IBD) and penetrate biological barriers to accumulate in vital organs beyond the gastrointestinal tract.
• Methodology: Researchers utilized a mouse model of ulcerative colitis, orally administering polystyrene particles—a common plastic found in food packaging—to analyze molecular and histological interactions with the intestinal mucosa and immune system.
• Mechanism of Action: MNP exposure triggers pro-inflammatory activation of macrophages and induces gut dysbiosis, characterized by a decrease in beneficial bacterial species and an increase in potentially harmful, pro-inflammatory microbes.
• Data Point: Nanoplastic particles smaller than 0.0003 millimeters (0.3 micrometers) demonstrated the highest mobility, successfully traversing the intestinal barrier to deposit in the liver, kidneys, and bloodstream.
• Contextual Findings: The uptake of MNPs into the intestinal mucosa is significantly intensified during active inflammatory states, suggesting a feedback loop where existing inflammation facilitates further plastic accumulation.
• Primary Implication: MNPs are an underestimated environmental factor in the pathogenesis of chronic inflammatory diseases, highlighting an urgent need to evaluate the systemic health risks posed by the migration of the smallest particles into major organ systems.

Cat Disease Challenges What Scientists Thought About Coronaviruses

Lychee had feline infectious peritonitis, a feline coronavirus. He was part of a clinical trial at the UC Davis School of Veterinary Medicine that cured him of the disease.
Photo Credit: Courtesy of University of California, Davis

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Researchers at UC Davis discovered that the feline coronavirus responsible for Feline Infectious Peritonitis (FIP) infects a much broader range of immune cells than previously believed, including B and T lymphocytes, rather than being limited to a single cell type.
• Methodology: The team examined lymph node samples from cats with naturally occurring FIP, analyzing the presence of viral material and evidence of active viral replication within specific immune cell populations.
• Mechanism: The study confirmed that the virus actively replicates inside these critical immune cells—B lymphocytes (antibody producers) and T lymphocytes (infection fighters)—instead of merely leaving behind inert fragments.
• Key Finding: Traces of the virus were found to persist in immune cells even after antiviral treatment was concluded and the cats appeared clinically healthy, suggesting a mechanism for disease relapse or long-term immune disruption.
• Implication: Because some immune cells have multi-year lifespans, this persistence offers a valuable model for understanding human long COVID and chronic post-viral syndromes, providing a rare opportunity to study viral reservoirs in immune tissues inaccessible in human patients.

The secret path of prostate infections

Confocal microscopy images showing that E. coli (red) preferentially adheres to luminal prostate cells (green) in human prostate tissue.
Image Credit: Maria Guedes & Carmen Aguilar

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Researchers elucidated the precise entry mechanism of Escherichia coli into prostate tissue, proving the invasion is a highly coordinated process targeting specific cell types rather than a random occurrence.
• Methodology: The team developed a novel "mini-prostate" organoid model using adult stem cells, which accurately replicates the architecture and cell diversity of human prostate epithelium to observe infection dynamics in real-time.
• Specific Detail/Mechanism: The infection utilizes a "lock-and-key" mechanism where the bacterial protein FimH binds specifically to the Prostatic Acid Phosphatase (PPAP) receptor found on the surface of luminal prostate cells.
• Key Statistic or Data: Laboratory experiments demonstrated that the sugar molecule D-mannose significantly reduced infection rates by acting as a "decoy," binding to bacterial FimH proteins and preventing them from attaching to host cells.
• Significance/Future Application: These findings identify D-mannose as a potential non-antibiotic therapeutic for bacterial prostatitis, addressing the critical need for alternatives to antibiotics in the face of rising resistance.
• Context: Bacterial prostatitis affects approximately 1% of the male population worldwide, with relapse rates exceeding 50% within a year despite long-term treatment with high-dose antibiotics.

How Wheat Fends Off Fungi

Photo Credit: Wolfgang Hasselmann

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Researchers at the University of Zurich identified a novel immune evasion strategy in wheat powdery mildew (Blumeria graminis), where the fungus employs a secondary effector protein specifically to mask the presence of a primary effector (AvrPm4) from the host's immune system.
• Biological Mechanism: Unlike typical resistance evasion—where pathogens mutate or discard detected proteins—this mechanism allows the fungus to retain the vital AvrPm4 effector by deploying a second "masking" effector that blocks recognition by the wheat resistance protein Pm4.
• Critical Interaction: The secondary masking effector exhibits a dual function; while it inhibits Pm4-mediated detection, it is simultaneously vulnerable to recognition by a separate, distinct wheat resistance protein, creating a potential "evolutionary trap."
• Experimental Application: Laboratory trials demonstrated that "stacking" the resistance gene for Pm4 with the gene targeting the secondary effector successfully neutralizes the pathogen, as the fungus cannot suppress one immune response without triggering the other.
• Significance: Published in Nature Plants (January 2026), this finding offers a blueprint for engineering durable wheat varieties that exploit interacting fungal effectors to significantly delay or prevent the "breakdown" of disease resistance in global agriculture.

New test shows which antibiotics actually work

Some bacterial pathogens play dead to dodge antibiotics. A new test watches them closely—and helps choose drugs that finish the job
Image Credit: Scientific Frontline / AI generated

Scientific Frontline: "At a Glance" Summary

• Researchers at the University of Basel and University Hospital Basel developed "antimicrobial single-cell testing," a novel method that precisely measures the lethality of antibiotics against bacteria rather than merely their ability to inhibit growth.
• The technique utilizes high-throughput microscopic imaging to film millions of individual bacteria under thousands of conditions over several days, tracking the survival and death kinetics of each cell in real-time.
• Validation involved testing 65 combination therapies on Mycobacterium tuberculosis and analyzing bacterial samples from 400 patients infected with Mycobacterium abscessus.
• Unlike traditional susceptibility tests that often fail to detect dormant bacteria capable of reviving post-treatment, this approach identifies "antibiotic tolerance," where pathogens survive exposure without reproducing.
• This technology enables personalized medicine by tailoring antibiotic regimens to a patient's specific bacterial strain and offers a more accurate predictor of therapeutic success than current clinical or animal model data.

What Causes Some People’s Gut Microbes to Produce High Alcohol Levels?

First author Cynthia Hsu examines a stool culture from a patient on an agar plate.
Photo Credit: UC San Diego Health Sciences

A study of people with a rare condition known as auto-brewery syndrome has found a link between gut microbes and symptoms of intoxication, pointing to new treatment strategies.

Researchers at University of California San Diego, Mass General Brigham, and their colleagues have identified specific gut bacteria and metabolic pathways that drive alcohol production in patients with auto-brewery syndrome (ABS). The rare and often misunderstood condition causes people to experience intoxication without drinking alcohol. The study was published in Nature Microbiology on January 8, 2026.

ABS occurs when gut microbes break down carbohydrates and convert them to ethanol (the alcohol found in intoxicating beverages), which then enters the bloodstream. While the metabolism of carbohydrates can produce small amounts of alcohol in everyone, levels can be high enough to cause intoxication in people with ABS. The condition is extremely rare but likely underdiagnosed due to a lack of awareness, diagnostic challenges, and stigma.

Escherichia albertii: The still unfolding journey of a misdiagnosed pathogen

Animal to human bacteria pathways
Escherichia albertii is primarily found in mammals and birds, suggesting it is a novel zoonotic pathogen.
Image Credit: Osaka Metropolitan University

Escherichia albertii, initially identified as Hafnia alvei, by the commercial identification biochemical strip, API 20E, was isolated from an infant with diarrhea in Bangladesh in 1989. However, this bacterium was later renamed as a novel species, E. albertii because of its similarities in biochemical and genetic properties to the genus Escherichia, but different from those of any known species in the genus. E. albertii possesses many pathogenic attributes including a key one, which is the ability to produce attaching and effacing (A/E) lesions in the intestinal mucosa mediated by genes on a 35-kb pathogenicity island called the locus of enterocyte effacement. Therefore, it is a member of the family of A/E pathogens.

Immune system keeps mucosal fungi in check

The yeast fungus Candida albicans (blue) breaks out of human immune cells (red) by forming long thread-like cells called hyphae. The part of the hypha that has already left the immune cells is colored yellow.
Image Credit: Erik Böhm, Leibniz-HKI

The yeast Candida albicans colonizes mucosal surfaces and is usually harmless. However, under certain conditions it can cause dangerous infections. A research team at the University of Zurich has now discovered how the immune system prevents the transformation from a harmless colonizer to a pathogenic mode. This happens, among other things, by sequestering zinc. 

The microbiome not only consists of bacteria, but also of fungi. Most of them support human and animal health. However, some fungi also have pathogenic potential. For instance, the yeast Candida albicans can grow in an uncontrolled manner on the oral mucosa, causing oral thrush. 

In severe cases by growing in a filamentous form, it can enter the bloodstream and cause systemic infections, which account for over one million deaths per year. This happens primarily in people with a weakened immune system on intensive care units, for instance individuals who are immunosuppressed because of a transplantation or cancer. 

How bacteria resist hostile attacks

Aggressor bacteria such as Acinetobacter baylyi (green) can rarely kill Pseudomonas aeruginosa (live cells in black, dying cells in cyan).
Image Credit: Alejandro Tejada-Arranz, Biozentrum, University of Basel

Some bacteria use a kind of molecular “speargun” to eliminate their rivals, injecting them with a lethal cocktail. Researchers at the University of Basel have now discovered that certain bacteria can protect themselves against these toxic attacks. But this defense comes with a surprising downside: it makes them more vulnerable to antibiotics. 

Countless bacterial species share cramped environments where competition for space and resources is fierce. Some rely on a molecular speargun to outcompete their opponents. One of them is Pseudomonas aeruginosa. It is widespread in nature but also notorious as a difficult-to-treat hospital pathogen. 

Pseudomonas can live peacefully in coexistence with other microbes. But when attacked by bacteria from a different species, it rapidly assembles its own nano-speargun – the so-called type VI secretion system (T6SS) – to inject its aggressor with a toxic cocktail. 

How can Pseudomonas strike back when it has already been hit by a deadly cocktail itself? The answer has now been uncovered by Professor Marek Basler’s team at the Biozentrum of the University of Basel and published in Nature Communications. 

New study reviews research linking probiotic and prebiotic supplements and skin health

Photo Credit: Christin Hume

Researchers from King’s College London and Yakult Science for Health have conducted a comprehensive review of existing research exploring how probiotic, prebiotic, and synbiotic supplements may influence skin health and disease.

The review mapped 516 studies from around the world examining the relationship between these supplements and various aspects of skin health, from general skin condition to the management of diseases such as atopic dermatitis, psoriasis, and acne. 

Our diet can influence skin health through its impact on the gut microbiome — the community of microorganisms living in our digestive tract. The concept of a gut–skin axis was first proposed nearly a century ago but has gained renewed attention in recent years, as growing evidence suggests that changes in gut microbes can affect skin condition and ageing. Probiotics, prebiotics, and synbiotics are thought to promote skin health by modifying the gut microbiome, which may in turn improve skin function and resilience. 

Microbiology: In-Depth Description

Image Credit: Scientific Frontline / AI generated

Microbiology is the scientific study of microorganisms, a diverse group of microscopic life forms that include bacteria, archaea, viruses, fungi, prions, protozoa, and algae. Collectively, these organisms function as the invisible backbone of the biosphere, influencing every ecosystem on Earth. The primary goal of this field is to understand the structure, function, genetics, and ecology of these entities, as well as their complex interactions with humans, other organisms, and the environment.

Microplastics pose a human health risk in more ways than one

Bio-beads collected near Truro.
Photo Credit Beach Guardian

A new study shows that microplastics in the natural environment are colonized by pathogenic and antimicrobial resistant bacteria. The study team calls for urgent action for waste management and strongly recommends wearing gloves when taking part in beach cleans. 

Microplastics are plastic particles less than 5mm in size and are extremely widespread pollutants. It is estimated that over 125 trillion particles have accumulated in the ocean (surface to seabed) and they have also been detected in soils, rivers, lakes, animals and the human body. 

An emerging concern associated with microplastics is the microbial communities that rapidly make their home on the particle surface, forming complex biofilms known as the “Plastisphere”. These communities may often include pathogenic (disease-causing) or antimicrobial resistant (AMR) bacteria. 

Why the "gut brain" plays a central role for allergies

This tissue section, taken from the intestine of a mouse unable to produce the neuropeptide VIP, clearly shows the striking frequency with which certain cell types occur on the intestine's surface. These include villous cells (red), mucus-producing goblet cells (yellow), Paneth cells (pink) and stem cells (green).
Image Credit: © Charité | Luisa Barleben

The intestinal nervous system, often referred to as the "gut brain", is essential in controlling digestion and maintaining the intestinal barrier. This protective layer, made up of the intestinal mucosa, immune cells and the microbiome, shields the body from the contents of the gut. Its effectiveness depends on the delicate balance among these components. If this balance is disrupted, inflammation, allergies, or chronic intestinal diseases can arise. The intestinal mucosa serves as the body’s primary defense against pathogens. While previous studies have shown that the intestinal nervous system is involved in immune responses in addition to digestion, its role in the development of intestinal epithelial cells has remained largely unclear until now. 

Stroke scientists gather more evidence for presence of ‘gut-brain axis’

Image Credit: Scientific Frontline / stock image

Research on mice by scientists at The University of Manchester has shed new light on why the guts’ immune system changes after a stroke and how it might contribute to gastro-intestinal problems. 

Published in Brain, Behavior and Immunity, the study adds to the emerging idea of the “gut-brain axis” – in which scientists suggest allows communication between the two organs in both health and disease. 

The study casts more light on the biology of stroke, a life-threatening medical emergency that disrupts blood flow to parts of the brain often causing long-term effects to mobility and cognition. 

Stroke patients are also at risk of secondary bacterial infections and often exhibit gastrointestinal symptoms including difficulty swallowing and constipation. 

Disrupting bacterial "chatter" to improve human health

Computer-rendered split image of bacteria on a tooth surface. When microbial communication is “on”, disease-associated species grow (left). Disrupting this communication (right) promotes health-associated bacteria.
Image Credit: University of Minnesota

Like all living things, bacteria adapt to survive. Over time, bacteria have been developing resistance to common antibiotics and disinfectants, which poses a growing problem for healthcare and sanitation. However, many species of bacteria are beneficial and even essential for human health. What if there was a way to change the behavior of bacteria in the body to prevent illness and poor health outcomes? 

Bacteria are very “talkative.” Constant streams of communication, known as quorum sensing, occur between and among the 700 species of bacteria that live in a human mouth. A number of them communicate via special molecules called N-acyl homoserine lactones (AHLs). 

A Microbial Blueprint for Climate-Smart Cows

Matthias Hess, with the UC Davis Department of Animal Science, and researchers at UC Berkeley, have identified which microbes in a cow's gut could help reduce methane. It brings them a step closer to engineering gut microbes to create more climate-friendly cows.
Photo Credit: Gregory Urquiaga / UC Davis

Each year, a single cow can belch about 200 pounds of methane. The powerful greenhouse gas is 27 times more potent at trapping heat in the atmosphere than carbon dioxide. For decades, scientists and farmers have tried to find ways to reduce methane without stunting the animal’s growth or productivity. 

Recent research at University of California, Davis, has shown that feeding cows red seaweed can dramatically cut the amount of methane that is produced and released into the environment. Until now, however, scientists did not fully understand how red seaweed changes the interactions among the thousands of microbes in the cow’s gut, or rumen. 

New analysis yields clearer picture of toxin-producing blue-green algae blooms

2024 cyanobacterial bloom at Detroit Reservoir
Photo Credit: Elijah Welch, city of Salem.

A long-term analysis shows that a major Oregon reservoir abruptly swapped one type of toxic algae for another midway through the 12-year study period, absent from any obvious cause. 

The project provides a novel look at harmful algal blooms, or HABs which pose multiple health risks to people and animals worldwide. 

Harmful algal blooms in lakes and reservoirs are explosions of cyanobacteria, often referred to as blue-green algae. Microscopic organisms ubiquitous in all types of water around the globe, cyanobacteria use sunlight to make their own food and in warm, nutrient-rich environments can quickly multiply, resulting in blooms that spread across the water’s surface. 

These blooms can form at any time of the year but most often occur between spring and fall. Some types of cyanobacteria produce liver toxins and neurotoxins, while others make toxins that can cause gastrointestinal illness if swallowed and acute rashes upon contact with skin.