Biochemistry lab at IU Bloomington finds chemical solution for tackling antibiotic resistance

“I love thinking outside the box when it comes to the antibiotic resistance problem,” said J.P. Gerdt, assistant professor of chemistry at Indiana University Bloomington.
Photo Credit: Chris Meyer, Indiana University

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Identification of a small chemical molecule that actively inhibits bacterial immune defenses, enabling bacteriophages to successfully infect and destroy bacteria that would otherwise resist viral attack.
• Methodology: Researchers screened a commercial compound library against a model bacterium to isolate specific molecules capable of suppressing the bacteria's immune response to bacteriophages.
• Key Data: The specific bacterial immune system mechanism targeted by the discovered molecule is present in approximately 2,000 distinct bacterial species.
• Significance: Offers a potential solution to antimicrobial resistance by potentiating phage therapy, allowing for the precise elimination of pathogens like Staphylococcus aureus without harming beneficial microbiomes, unlike broad-spectrum antibiotics.
• Future Application: Development of a comprehensive library of bacterial immune inhibitors over the next 10 to 15 years for use in agriculture and treating hard-to-cure human infections.
• Branch of Science: Biochemistry and Microbiology
• Additional Detail: These findings were published in the journal Cell Host and Microbe in a paper titled "Chemical inhibition of a bacterial immune system."

Multiple bacteria may be behind elk hoof disease

New research from WSU's College of Veterinary Medicine found that multiple bacteria, rather than a single pathogen, is driving elk hoof disease among Northwestern herds
Photo Credit: Byron Johnson

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Treponeme-associated hoof disease (TAHD) in elk is driven by a polymicrobial community rather than a single pathogen, with Mycoplasma species identified as a critical coinfector alongside the previously known Treponema spirochetes.
• Methodology: Researchers performed a comparative analysis of hoof tissue samples from 129 free-ranging elk across regions with varying disease prevalence, screening for bacterial presence in both lesioned and healthy tissues.
• Key Data: Treponema and Mycoplasma were consistently detected in all diseased samples but were entirely absent in healthy hooves, with no significant statistical difference in bacterial community composition between areas of high versus sporadic disease rates.
• Significance: The confirmation of a complex, multi-bacterial etiology explains the difficulty in managing the disease and suggests that bacterial synergy, rather than a single agent, drives tissue destruction and disease progression.
• Future Application: These findings will facilitate the development of new diagnostic assays capable of detecting TAHD in live animals, moving away from the current reliance on post-mortem tissue analysis.
• Branch of Science: Veterinary Microbiology and Wildlife Epidemiology.
• Additional Detail: Associated bacteria, including Fusobacterium and Corynebacterium, were also linked to lesions, further supporting the conclusion that the disease manifests through a consistent, stable community of microbes regardless of geographic location.

A debilitating hoof disease affecting elk herds across the Pacific Northwest appears to be driven not by a single pathogen but by multiple bacterial species working together, according to a study led by researchers in Washington State University’s College of Veterinary Medicine.

How genes influence the microbes in our mouths

Illustration Credit: Agnieszka Grosso

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Scientists identified 11 specific regions of the human genome that significantly influence the composition and abundance of oral microbial communities, confirming that host genetics play a critical role in determining the mouth's bacterial environment.
• Methodology: Researchers analyzed whole-genome sequences derived from saliva samples of over 12,500 individuals, repurposing the data to simultaneously measure human genetic markers and the abundance of 439 common microbial species.
• Key Data: The study found that the FUT2 gene variant affected the levels of 58 oral bacterial species, while variations in the AMY1 gene influenced the abundance of more than 40 species.
• Significance: This research establishes a direct biological link between human genetics and oral health, suggesting that genetic factors can predispose individuals to cavities and tooth loss by altering the oral microbiome, independent of dental hygiene habits.
• Future Application: The statistical methods and findings developed in this study lay the groundwork for personalized dental care strategies and further large-scale investigations into how human genetics shape microbiomes throughout the body.
• Branch of Science: Genomics, Microbiology, and Oral Biology
• Additional Detail: Individuals with higher copy numbers of the AMY1 gene, which encodes a starch-digesting enzyme, showed increased populations of sugar-feeding bacteria and a statistically significant correlation with higher rates of denture use.

Scientists find hidden diversity inside common brain parasite

Toxoplasma gondii primarily infects the epithelial cells of a cat's small intestine
Image Credit: Scientific Frontline

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Toxoplasma gondii brain cysts, previously believed to contain a single uniform type of dormant parasite, actually harbor at least five distinct subtypes with specialized roles in survival, spread, and reactivation.
• Methodology: Researchers utilized advanced single-cell RNA sequencing to analyze individual parasites isolated directly from cysts within the brains of mice, a model chosen to closely mirror natural chronic infection.
• Key Data: The study identified at least five functionally distinct subtypes of bradyzoites within cysts that can reach up to 80 microns in diameter; this parasite currently infects approximately one-third of the global human population.
• Significance: This finding reshapes the understanding of the parasite's life cycle from a simple linear model to a complex network, explaining why current treatments fail to eliminate cysts and how the parasite persists for life.
• Future Application: These results identify specific parasite subtypes primed for reactivation, offering precise targets for novel therapeutic drugs capable of eradicating chronic infection rather than just managing acute symptoms.
• Branch of Science: Biomedical Sciences / Parasitology

More Than Just Gut Cohabitants: How Gut Bacteria Control Immune Responses

The gut-brain axis is a bidirectional communication network linking the central nervous system with the enteric nervous system (the "second brain" in the gut) via neural, hormonal, and immune pathways.
Image Credit: Scientific Frontline / stock image

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Commensal gut bacteria utilize type III secretion systems, previously thought exclusive to pathogens, to inject effector proteins directly into human cells and actively manipulate host immune responses.
• Methodology: The research consortium constructed a large-scale interactome map identifying over 1,000 protein-protein interactions between bacterial effectors and human host proteins, validated by functional assays of immune signaling pathways.
• Key Data: Analysis revealed that genes encoding these secretion systems are significantly enriched in the microbiomes of patients with Crohn’s disease, with specific proteins targeting the NF-κB signaling pathway and cytokine responses.
• Significance: These findings fundamentally shift the understanding of the microbiome from correlation to causation, demonstrating that non-pathogenic bacteria are active agents capable of directly modulating human physiology and inflammation.
• Future Application: This mechanistic insight facilitates the development of targeted therapeutic strategies that modulate specific bacterial-host interactions to treat inflammatory bowel diseases and potentially other autoimmune disorders.
• Branch of Science: Microbiology, Immunology, and Network Biology
• Additional Detail: The study specifically highlights the modulation of Tumor Necrosis Factor (TNF) activity, a key cytokine in inflammation, providing a molecular basis for the efficacy of anti-TNF therapies in Crohn's disease.

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.