Researchers at University of California San Diego School of Medicine used bacteria found on healthy cats to successfully treat a skin infection on mice. These bacteria may serve as the basis for new therapeutics against severe skin infections in humans, dogs and cats.
The study, published in eLife on October 19, 2021, was led by Richard L. Gallo, MD, PhD, Distinguished Professor and chair of the Department of Dermatology at UC San Diego School of Medicine, whose team specializes in using bacteria and their products to treat illnesses — an approach known as “bacteriotherapy.”
Skin is colonized by hundreds of bacterial species that play important roles in skin health, immunity and fighting infection. All species need to maintain a diverse balance of healthy skin bacteria to fight potential pathogens.
“Our health absolutely depends on these ‘good’ bacteria,” said Gallo. “They rely on our healthy skin to live, and in return some of them protect us from ‘bad’ bacteria. But if we get sick, ‘bad’ bacteria can take advantage of our weakened defenses and cause infection.”
This is the case with methicillin-resistant Staphylococcus pseudintermedius (MRSP), a bacterium commonly found on domesticated animals that becomes infectious when the animals are sick or injured. MRSP is an emerging pathogen that can jump between species and cause severe atopic dermatitis, or eczema. These infections are common in dogs and cats, and can also occur in humans, though rates of human infection vary around the world. As its name suggests, MRSP is resistant to common antibiotics and has been difficult to treat in clinical and veterinary settings.
To address this, researchers first screened a library of bacteria that normally live on dogs and cats and grew them in the presence of MRSP. From this, they identified a strain of cat bacteria called Staphylococcus felis (S. felis) that was especially good at inhibiting MRSP growth. They found that this special strain of S. felis naturally produces multiple antibiotics that kill MRSP by disrupting its cell wall and increasing the production of toxic free radicals.

Some viral diseases could possibly contribute to neurodegeneration. DZNE researchers report this in the scientific journal Nature Communications. Their assessment is based on laboratory experiments in which they were able to show that certain viral molecules facilitate intercellular spreading of protein aggregates that are hallmarks of brain diseases like Alzheimer’s. These findings may provide clues how acute or chronic viral infections could contribute to neurodegeneration.
Aggregates of misfolded proteins, which occur in so-called prion diseases such as Creutzfeldt-Jakob disease, have the ability to pass from one cell to another, where they transfer their abnormal shape to proteins of the same kind. As a result, the disease spreads across the brain. A similar phenomenon is discussed for Alzheimer’s and Parkinson’s disease, which also exhibit assemblies of misfolded proteins. Transmission of aggregates could involve direct cell-to-cell contact, the release of “naked” aggregates into extracellular space or packaging in vesicles, which are tiny bubbles surrounded by a lipid envelope that are secreted for communication between cells. “The precise mechanisms of transmission are unknown,” says Ina Vorberg, a research group leader at the DZNE’s Bonn site and professor at the University of Bonn. “However, it is an obvious guess, that aggregate exchange by both direct cell contact and via vesicles depends on ligand-receptor interactions. This is because in both scenarios, membranes need to make contact and fuse. This is facilitated when ligands are present that bind to receptors on the cell surface and then cause the two membranes to fuse.”
Experiments with Cell Cultures
Based on this assumption, Vorberg’s team, with support from DZNE colleagues in Munich and Tübingen as well as Belgian scientists, performed an extensive series of studies with different cell cultures. Thereby, they investigated the intercellular transfer of either prions or aggregates of tau proteins, as they occur in similar form in prion diseases or Alzheimer’s disease and other “tauopathies.” Mimicking what happens as a result of viral infection, the researchers induced cells to produce viral proteins that mediate target cell binding and membrane fusion. Two proteins were chosen as prime examples: SARS-CoV-2 spike protein S, which stems from the virus causing COVID-19, and vesicular stomatitis virus glycoprotein VSV-G, which occurs in a pathogen that infects cattle and other animals. Moreover, cells expressed receptors for these viral proteins, namely the LDL receptor family, which act as docking ports for VSV-G, and human ACE2, the receptor for the spike protein.
Ligands Facilitate Aggregate Spreading
“We could show that the viral proteins are incorporated both into the cellular membrane and into the extracellular vesicles. Their presence increased protein aggregate spreading between cells, both by direct cell contact or by extracellular vesicles. The viral ligands mediated an effective transfer of aggregates into recipient cells, where they induced new aggregates. The ligands act like keys that unlock the recipient cells and thus sneak in the dangerous cargo,” Vorberg says. “Certainly, our cellular models do not replicate the many aspects of the brain with its very specialized cell types. However, independent of the tested cell type producing the pathologic aggregates, the presence of viral ligands clearly increased the spreading of misfolded proteins to other cells. All in all, our data suggests that viral ligand-receptor interactions can in principle affect transmission of pathologic proteins. This is a novel finding.”
Potential Effects on Neurodegeneration
“The brains of patients suffering from neurodegenerative diseases sometimes contain certain viruses. They are suspected to cause inflammation or to have a toxic effect, thus accelerating neurodegeneration. However, viral proteins could also act differently: They could increase intercellular spreading of protein aggregates already ongoing in neurodegenerative diseases like Alzheimer’s,” Vorberg says. “Of course, this needs further studies with neurotropic viruses. Clearly, the impact of viral infections on neurodegenerative diseases deserves in-depth investigation.”

A team of researchers at Georgia State University has developed a novel approach for detecting the activity of calcium within cells. The study, led by Regents’ Professor of Chemistry Jenny Yang, demonstrates the effectiveness of a red biosensor that can directly monitor calcium at specific locations within a cell, a discovery that could aid in better understanding of the molecular basis of human diseases.
Calcium is essential for many physiological processes, including the health and function of the muscular, nervous, circulatory and digestive systems. Calcium amplifies signaling molecules that prompt a response inside cells, controls the release of neurotransmitters (chemical messengers that transmit signals from neurons), triggers the contraction of muscle cells and aids in fertilization. Calcium is also important for proper bone formation, and many processes within cells require or use calcium.
Given this wide range of functions, calcium movement and levels can serve as good indicators for biological mechanisms and changes. However, previous attempts at developing calcium sensor tools that can monitor rapid signaling changes have proven limiting due to slow responses of the sensors reported.
“The challenge is how to capture these quick changes in very specific locations,” said Yang, who is also the associate director of the Center for Diagnostics and Therapeutics and director of Advanced Translational Imaging Facility. “For example, if I have an injury in my muscle, there’s a specific muscle cell calcium change and it happens very fast.”
To better capture these signals, Yang and her colleagues have created a way to design a calcium binding site onto the surface of several fluorescent proteins. The study, published in the journal Angewandte Chemie, shows that the red calcium sensor, known as R-CatchER, is highly sensitive at detecting calcium signals in multiple cell types. The discovery is a breakthrough by Yang and her team, who have spent decades developing and refining their technique. They recently published a paper on the development of a green calcium sensor, known as G-CatchER+, in the journal iScience.
“The protein we’re using is able to identify fleeting changes and directly measure calcium activity,” said Yang. “We can monitor calcium events in healthy cells and see how they change in disease states.”
Ultimately R-CatchER could be useful for laboratory research and studies; for example, determining whether there is a connection between changes in calcium and a particular disease. Their technology could also aid in drug discovery.
“We have a unique approach to understanding how aging events or disease states are controlled by calcium. This tool could tell scientists exactly which signal pathway is related to a disease and how it changes when treated with a drug compound,” Yang said. “It could show the specific location that the drug needs to target to be effective.”
The researchers say the next step is to apply the technology in animal models to help better understand how various cell events are involved in disease.
Yang is known as a pioneer in the field she calls “calciomics,” which incorporates protein chemistry, biology, cell biology and neuroscience to develop computational studies and calcium sensor tools. In 2019, she was selected as National Academy of Inventors Fellow in honor of her work.
Co-authors of the study include chemistry doctoral student Xiaonan Deng, Donald Hamelberg, professor of chemistry, and Xinqiu Yao, postdoctoral associate in chemistry.
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Chemicals used to “grease proof” everything from food packaging to carpets have built up in the environment for decades and contaminate ecosystems across the globe, and a new study is calling for a better understanding of the risks posed by these chemicals.
The study, published in the academic journal Trends in Food Science & Technology, collects the proceedings of a symposium chaired by an Iowa State University scientist and issued a call to action on the need for new and better ways to detect and mitigate this class of chemical compounds, collectively known as per- and polyfluoroalkyl substances (PFAS). Evidence indicates exposure to high levels can lead to adverse health effects for humans and other species, and the study stresses the need for new ways to measure and study exposures to these synthetic chemicals from various sources including food.
PFAS accumulate in the environment and do not break down on their own. For instance, the compounds can contaminate waterways after leaching from products discarded in landfills, said Keith Vorst, director of the Polymer and Food Protection Consortium and an associate professor of food science and human nutrition at Iowa State. These entirely humanmade chemicals have been used in a wide range of products since the 1940s, and some states have enacted legislation to restrict their use. But their ability to persist in the environment means the compounds that already exist can continue to contaminate the environment.
“They’re out there, we need to be aware of them, and it’s really hard to eliminate them,” Vorst said. “We need to work on mitigation strategies, and we need to be monitoring them and better understand the risks they pose.”
What are PFAS? PFAS often have been used to coat food packaging as a barrier to keep grease from escaping. Vorst said paper wrappers on hamburgers are often coated in these compounds to prevent grease from leaking onto consumers’ hands. The compounds have also been used widely to coat carpets, in car interiors and in fire-fighting foams.
Some PFAS are no longer produced in the United States, but Vorst said more than 5,000 separate compounds qualify under this category, making it difficult for regulations to keep up with newly developed chemicals.
Studies have indicated that exposure to high levels of some of these chemicals can cause reproductive and developmental, liver and kidney, and immunological effects in laboratory animals, according to the Environmental Protection Agency. The EPA reports the most consistent findings are increased cholesterol levels among exposed populations, and studies have found limited evidence for links between high levels of certain PFAS and low infant birth weights, effects on the immune system, cancer and thyroid hormone disruption.
Monitoring and mitigation The new paper emerged out of a virtual symposium held in June of 2020 organized by the Institute for the Advancement of Food and Nutrition Sciences. The symposium featured scientists, engineers and regulatory professionals from public, private and academic institutions. The symposium addressed science gaps for exposure routes, detection and quantification of PFAS in food. Speakers also noted that, based on limited data to date, there is little PFAS detected in food.
Polymer and Food Protection Consortium researchers Greg Curtzwiler, an assistant professor of food science and human nutrition, and Paulo Silva, adjunct assistant professor of food science and human nutrition, are working with Vorst in the laboratory to study potential mitigation strategies such as high voltage atmospheric cold plasma to change the chemistry of PFAS. This process could work by passing materials that contains PFAS, such as product packaging or even drinking water, through an engineered atmosphere to mitigate the compounds. The research team has tested the method and is working with Iowa State to patent the technology. Vorst’s PFPC lab has been testing new methodologies to detect and monitor PFAS levels in various environments as well. Much of this research was funded by the ISU Polymer and Food Protection Consortium.
“We’re looking at continuous monitoring of exposure limits,” Vorst said. “We’re trying to develop threshold limits for packaging and products. We’re also looking at how we can change these chemistries to get them out of the environment, make them less persistent or sequester them.”
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A spinal cord injury damages the lines of communication between the body and brain, impeding the signals that drive movement and sensation. Injured motor and sensory neurons in the central nervous system — the brain and spinal cord — have limited ability to heal, so people who survive such injuries can be left with chronic paralysis, numbness and pain.
Researchers at Washington University School of Medicine in St. Louis have identified a drug that helps sensory neurons in the central nervous system heal. Neurons are surrounded by support cells that protect and nurture them. In this study, the researchers gave mice with injured sensory neurons a drug called fenofibrate that is approved by the Food and Drug Administration to treat high cholesterol. The drug activated the support cells surrounding sensory neurons and helped them regrow about twice as fast as sensory neurons in mice that received a placebo. The study is available online in eLife.
“When people think of spinal cord injury, they tend to think of paralysis, but there are a lot of problems with sensory processing and pain after spinal cord injury as well,” said senior author Valeria Cavalli, PhD, the Robert E. and Louise F. Dunn Professor of Biomedical Research and a professor of neuroscience. “Addressing those sensory issues could go a long way toward improving quality of life for survivors. Our data indicate that fenofibrate has the potential to activate these support cells and improve recovery, which means we could potentially repurpose this FDA-approved compound to help restore sensory function after nerve injuries.”
Unlike neurons in the brain or spinal cord, sensory nerves in the periphery of the body heal after injury, which is why a gash on your leg doesn’t leave part of your leg permanently numb. To understand why regeneration occurs in the peripheral but not the central nervous system, Cavalli studies a unique cell type that spans both systems: sensory neurons of the dorsal root ganglia. The cell bodies of such neurons bundle together into a structure known as a ganglion that sits just outside the spinal cord. A long, thin arm called an axon branches out from each cell body in opposite directions, with one branch heading into the central nervous system via the spinal cord and the other becoming part of the peripheral nervous system as it descends into the body. Despite being two parts of the same cell, the peripheral and central axonal branches do not respond identically after injury. The peripheral parts regrow and recover much faster and more completely than the central ones.
Cavalli and first author Oshri Avraham, PhD, a staff scientist, suspected that the differences in regeneration between the two branches may come down to differences between the behavior of support cells in response to injury to the central versus peripheral axon branches.
To investigate that possibility, the researchers compared gene expression in five kinds of support cells in the ganglion, after injury to the peripheral and central branches of the sensory neuron. They found that the patterns of gene expression in the support cells differed depending on which part of the neuron they injured. Most notably, so-called satellite glial cells ramped up expression of a set of genes known as the PPAR-alpha pathway — famous for its role in fat metabolism — only after injury in the peripheral axon branch. The pathway was not turned up after injury to central axonal branches, and was actually dialed down after spinal cord injury in the central nervous system.
To Cavalli and Avraham, this observation suggested that the PPAR-alpha pathway may promote regeneration. To find out, they fed mice fenofibrate — a drug that activates PPAR alpha — for two weeks before injuring the mice’s sensory axon branch heading into the central nervous system. Three days after the injury, the central branches of the sensory neuron axons had regrown about twice as much in the mice that had received fenofibrate than in those that had received a placebo.
“PPAR alpha is only expressed in satellite glial cells, not in neurons, so these results tell us that targeting these support cells can improve regeneration and potentially relieve sensory symptoms like pain,” Cavalli said. “It gives us an additional tool to design therapies to restore function after nerve injuries. We haven’t fixed spinal cord injury, but we’re one step closer to figuring out how to do it.”
Cavalli and colleagues are now planning experiments to combine fenofibrate with other experimental regeneration-promoting therapies targeting neurons or other aspects of the central nervous system to further enhance regeneration.
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Materials provided by Washington University School of Medicine. Original written by Tamara Bhandari. Note: Content may be edited for style and length.

Tangles in unwound DNA can create mutational hotspots in the genomes of bacteria, according to a new study by the Milner Centre for Evolution at the University of Bath. The study authors say these findings will help us in the future to predict the evolution of bacteria and viruses over time, which could aid vaccine design and better understanding of antibiotic resistance.
While most evolution is shaped by natural selection, where only those individuals who are adapted for their environment are able to survive and pass on their genes, a new study published in Nature Communications shows that evolution is also influenced by tangles in the DNA strands.
A team of scientists, led by the University of Bath in collaboration with the University of Birmingham, looked at the evolution of two strains of the soil bacteria Pseudomonas fluorescens (SBW25 and Pf0-1).
When the scientists removed a gene that enables the bacteria to swim, both strains of the bacteria quickly evolved the ability to swim again, but using quite different routes.
One of the strains (called SBW25), always mutated the same part of a particular gene to regain mobility.
However, the other strain (called Pf0-1) mutated different places in different genes each time the scientists repeated the experiment.

A collaboration among microbiologists, clinicians and experts on bacterial evolution revealed that, with time, highly adapted bacterial communities in the sinuses of people with cystic fibrosis (CF) become more fragmented and experience mutations that erode their genomes — a dogma-challenging discovery that has scientists reimagining how they think about the evolution of microbes in chronic infections.
In a paper published today in Cell Reports, researchers from the University of Pittsburgh School of Medicine announce their discovery that the size and structure of populations of the pathogenic bacterium Pseudomonas aeruginosa vary widely in the sinuses. They found that this so-called biogeography at the site of infection fundamentally impacts how bacteria evolve during chronic infections.
“A long-standing lore in the cystic fibrosis field says that each patient’s infection tells a unique story, and that Pseudomonas evolves in unpredictable ways,” said Jennifer Bomberger, Ph.D., associate professor at Pitt. “By using tools of evolutionary biology, we showed that a complicated and unwieldy field could be simplified — these microbes follow general trends that are rooted in evolutionary biology and studying those trends can help us create more effective interventions.”
Cystic fibrosis is an incurable genetic disease that affects tens of thousands of people all over the globe and manifests itself in the accumulation of thick, sticky mucus in the lungs. Because their immune systems are compromised, CF patients also suffer from frequent bacterial and fungal infections — which infiltrate the patient’s sinuses first and then spread into the lower respiratory tract, where they wreak havoc and can compound existing breathing problems.
Yet even though bacterial infections are associated with worse disease outcomes in patients with CF, doctors know little about how those infections get established in the first place.
“The sinuses are like the Wild West,” said lead author Catherine Armbruster, Ph.D., M.P.H., a postdoctoral fellow at Pitt. “It is striking how little we know about Pseudomonas’s evolution in the upper respiratory tract. There is no clear guidance on how to treat chronic sinus infections in cystic fibrosis. Even though these sinus infections probably seed bacteria down into the lungs, it’s unclear if and how those two populations interact.”
Inspired by research on ancient relationships between bacteria and their insect hosts, the researchers used advanced genome studies and state-of-the-art imaging techniques to analyze populations of P. aeruginosa taken from the sinuses of people with CF.

In many parts of the world, the supply of COVID-19 vaccines continues to lag behind the demand. While most vaccines are designed as a two-dose regimen, some countries, like Canada, have prioritized vaccinating as many people as possible with a single dose before giving out an additional dose.
In Chaos, by AIP Publishing, researchers from the Frankfurt School of Finance and Management and the University of California, Los Angeles illustrate the conditions under which a “prime first” vaccine campaign is most effective at stopping the spread of the COVID-19 virus.
The prime first campaign does not suggest people should receive only one dose of the vaccine. Instead, it emphasizes vaccinating large numbers of people as quickly as possible, then doubling back to give out second doses. In comparison, the “prime boost” vaccine campaign prioritizes fully vaccinating fewer people.
Immunologically speaking, the prime boost scenario is always superior. However, under supply constraints, the advantages of vaccinating twice as many people may outweigh the advantages of a double dose.
The scientists simulated the transmission of COVID-19 with a susceptible, exposed, infected, recovered, deceased model. Each of these disease states is associated with a compartment containing individual people. Transitions between compartments depend on disease parameters like virus transmissibility.
Each compartment is further divided to account for unvaccinated, partially vaccinated, and fully vaccinated individuals. The researchers measured how each vaccine group compared to the others under different conditions.
“We have this giant degree of uncertainty about the parameters of COVID-19,” said author Jan Nagler. “We acknowledge that we don’t know these precise values, so we sample over the entire parameter space. We give a nice idea of when prime first campaigns are better with respect to saving lives than prime boost vaccination.”
The team found the vaccine waning rate to be a critically important factor in the decision. If the waning, or decrease in vaccine effectiveness, is too strong after a single dose, the double dose vaccination strategy is often the better option.
However, the vaccine strategy flips if the waning rate after a single dose is more like the waning rate after a double dose.
“Our results suggest that better estimates of immunity waning rates are important to decide if prime first protocols are more effective than prime boost vaccination,” said author Lucas Böttcher.
As the scientific community gathers more data on COVID-19 vaccinations, the scientists hope this model will become more informative for public health experts and politicians who must decide for or against a certain vaccination protocol.
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Along with the use of face masks, social distancing in public remains one of the most practiced front-line defenses against the spread of COVID-19. However, flows of pedestrians, including those practicing the 6-foot rule for distancing, are dynamic and characterized by nuances not always carefully considered in the context of everyday, public spaces.
In Physics of Fluids, by AIP Publishing, researchers from Carnegie Mellon University examine the dynamics of social distancing practices through the lens of particle-based flow simulations. The study models social distance as the distance at which particles, representing pedestrians, repel fellow particles.
“Even at modest pedestrian density levels, a strong preference for 6 feet of social distance can cause large-scale pedestrian ‘traffic jams’ that take a long time to clear up,” said Gerald J. Wang, of Carnegie Mellon University. “This is pretty evident to all of us who have engaged in that ‘awkward dance of social distance’ in a grocery store aisle during the past 18 months, but it has important implications for how we set occupancy thresholds as workplaces, campuses, and entertainment venues return to pre-pandemic densities.”
Motivated by the pandemic, the researchers shed light on the relationship between social distancing and pedestrian flow dynamics in corridors by illustrating how adherence to social distancing protocols affects two-way pedestrian movement in a shared space. The results add to a significant body of recent work around the effects of various factors on pedestrian counterflows and focuses on the characterization of jamming phenomena in relatively narrow corridors, a topic of current interest.
“Dense pedestrian flows plus social distancing recommendations is a recipe for a lot of frustration,” said Wang. “I mean this both in the physics sense of the word ‘frustration,’ with low particle mobilities because a bunch of ‘stuff’ is seemingly in their way, and in the everyday sense of the word ‘frustration,’ with people feeling flustered because, well, a bunch of ‘stuff’ is seemingly in their way!”
Wang noted public health messaging should be aligned with realistic, achievable behavior, adding that “strict adherence to social distancing — a la ‘the 6-foot rule’ — is simply not a practical recommendation in pedestrian flows at densities that are typical of large, shared venues.”
Though conceptually easy to digest, the findings underscore the complications of applying a “one-size-fits-all” policy recommendation to a public sphere characterized by nuanced pedestrian flow dynamics.
“Particle-based flow simulation, powered by high-performance computing, has enormous potential to rapidly explore a broad range of pedestrian flow problems, both during the pandemic and beyond,” said co-author Kelby B. Kramer.
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The United States Centers for Disease Control and Prevention have suggested that smokers who are unable to quit smoking may benefit by switching from smoking cigarettes to vaping e-cigarettes if they switch completely and are able to avoid relapsing to cigarette smoking.
However, there have been few studies on whether smokers are able to transition to e-cigarettes — battery-operated devices that heat a liquid made of nicotine, flavorings and other chemicals to make an aerosol that users inhale into their lungs — without relapsing back to cigarette smoking.
Published in the Oct. 19, 2021 online issue of JAMA Network Open, an analysis by the Herbert Wertheim School of Public Health and Human Longevity Science at University of California San Diego and UC San Diego Moores Cancer Center reports that e-cigarette use — even on a daily basis — did not help smokers successfully stay off cigarettes.
“Our findings suggest that individuals who quit smoking and switched to e-cigarettes or other tobacco products actually increased their risk of a relapse back to smoking over the next year by 8.5 percentage points compared to those who quit using all tobacco products,” said first author John P. Pierce, Ph.D., Distinguished Professor at the Herbert Wertheim School of Public Health and UC San Diego Moores Cancer Center.
“Quitting is the most important thing a smoker can do to improve their health, but the evidence indicates that switching to e-cigarettes made it less likely, not more likely, to stay off of cigarettes.”
Researchers used data from the nationally representative Population Assessment of Tobacco and Health (PATH) longitudinal study, undertaken by the National Institute on Drug Abuse (NIDA) and the FDA Center for Tobacco Products under contract with Westat. The team identified 13,604 smokers between in 2013 and 2015 who were followed over two sequential annual surveys to explore changes in use of 12 tobacco products.