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How dietary restriction rewires immunity to protect against infection

To understand the complex interactions involved in an immune response during scarcity, the team put mice on a 50% restricted-calorie diet and then exposed the animals to bacteria that infect the gut. The mice that were fed a standard diet experienced a metabolic crash— their blood glucose levels and body weight plummeted.

The researchers had expected this would happen to all the animals because mounting an immune response can consume up to 30% of the entire body’s fuel reserves. But in the calorie-restricted mice, the immune system appeared to be functioning perfectly well without using much glucose.

To unravel this enigma, the researchers inventoried the immune cells of the infected animals and discovered that T cells, which normally target invading microbes, were depleted in the calorie-restricted mice. Instead, short-lived neutrophils, which serve as the body’s first responders to infection, were ramped up to twice the normal amount and had measurably enhanced pathogen-killing abilities. The cells seemed to be operating in energy-saving mode, consuming much less glucose than neutrophils from well-fed animals.

The researchers are breaking new ground by outlining how a sudden fall in food intake triggers glucocorticoid levels to rise, resulting in two major shifts. First, the body repositions certain immune cells—especially naïve T cells—into the bone marrow, which becomes a kind of “safe house” for when the cells are needed. Second, during an infection, glucocorticoids tilt the immune response away from energy-intensive T cells toward neutrophils, abundant cells that act as immediate, short-lived defenders.

Beyond clearing a current infection, glucocorticoids prepare the immune system for repeat encounters with infectious agents. While the hormones direct killer T cells to stand down and neutrophils to step up, they also ensure memory T cells are preserved for future confrontations.


When food is scarce, stress hormones direct the immune system to operate in “low power” mode to preserve immune function while conserving energy, according to researchers. This reconfiguration is crucial to combating infections amid food insecurity.

NAD+ sensing by PARP7 regulates the C/EBPβ-dependent transcription program during adipogenesis

Stokes et al. demonstrate that PARP7 “senses” the levels of nuclear NAD+ during early adipogenic differentiation via an ADP-ribosylation-ubiquitin-proteasome pathway to regulate C/EBPβ-dependent proadipogenic gene expression through p300-mediated H3K27 acetylation. Stabilized PARP7 promotes the binding of C/EBPβ to chromatin genome-wide, enhancing lipid synthesis and adipogenesis in vivo.

Genetic defect that weakens esophageal lining identified!

But the molecular factors responsible for the onset of Barrett’s esophagus remain poorly understood.

The findings, published in Nature Communications, combined family studies, laboratory experiments and genetically engineered mouse models to identify and understand how genetic defects contribute to disease development.

The team sequenced and analyzed genetic material of 684 people from 302 families where multiple members developed Barrett’s esophagus or esophageal cancer. They discovered that a subset of affected family members carry inherited mutations in a gene called VSIG10L.

“We found that this gene acts like a quality control system for the esophageal lining,” said the lead researcher. “When it’s defective, the cells do not mature properly and the protective barrier in the esophageal lining becomes weak, allowing stomach bile acid to cause tissue changes that enhances the risk of developing Barrett’s esophagus.”

When researchers genetically engineered mice with human-equivalent VSIG10L mutations, they found that the esophageal lining became disrupted structurally and molecularly, according to the author. The study found that when the mice were exposed to bile acid, they developed Barrett’s-like disease over time, effectively replicating the disease’s progression in humans.

These genetically engineered mice also represent the first animal model for Barrett’s esophagus based directly on human genetic predisposition to the disease, the author said.

With VSIG10L shown to be a key gene in maintaining esophageal health, family members can now be screened for genetic variants to identify those at a high-risk of developing Barrett’s esophagus or esophageal cancer. ScienceMission sciencenewshighlights.

System isolates single extracellular vesicle surface proteins to map function

Extracellular vesicles (EVs) are tiny biological bubbles that carry nucleic acids and proteins between cells, playing an essential role in tissue repair, neuroprotection and immune health. By isolating the surface proteins of these bubbles, researchers can understand more about their biology and build tools to transform extracellular vesicles into next-generation drugs for cancer, neurological conditions and other diseases.

UC Davis biomedical engineers are using EVs to crack the code of the body’s message system. Their findings are detailed in a paper published in ACS Nano.

“EV-mediated intercellular communication is a very powerful system that controls many physiological and pathophysiological phenomena,” said Aijun Wang, a corresponding author of the new study. Wang is Chancellor’s Fellow and professor of biomedical engineering and surgery. “We know that EVs are therapeutically useful. But how do we define what dictates their functions?”

Researchers copy viral strategies to get mRNA medicines into cells in one piece

Drugs made of mRNA have the potential to transform medicine—if only they could get into cells in one piece. Now, University of Connecticut researchers have shown that packaging mRNA like a virus could smuggle it into cells safely, opening up a new way to deliver mRNA into cells to treat diseases such as cancer. Their research is published in the journal ACS Nano.

Messenger RNA (mRNA) is a single strand of ribonucleic acids that tells the protein-making machinery inside cells what to do. Usually RNA strands are made using the DNA blueprints inside a cell’s central nucleus, and then travel out to the protein production areas. Getting a medicinal mRNA into a cell from outside, though, is another matter. Most things trying to enter a cell have to pass through an endosome. An endosome is like a decontamination bubble. Its interior becomes acidic, which activates enzymes that chew up anything potentially dangerous—like foreign RNA.

But many viruses have evolved to hijack this system.

Sunray-like ripples emerge on a frozen reaction front

Researchers in Belgium have unveiled a striking chemical reaction in which ripples along a frozen reaction front resemble the rays of a shining star. Publishing their results in Physical Review Letters, Anne De Wit and colleagues at the Université Libre de Bruxelles have shed new light on the patterns that emerge in reaction–diffusion systems, offering fresh insight into how similar structures arise in the natural world.

From forest fires to the spread of infectious diseases, many natural processes involve a “front” forming between two distinct states: be they burned and unburned forest, infected and healthy individuals, or any number of other examples in which one state spreads by consuming another.

Such behavior is often described using reaction–diffusion systems, where local reactions are coupled to transport processes such as diffusion. In the lab, this mechanism can be recreated by injecting a chemical compound into the center of a circular chamber filled with another reactant. If the chemistry is autocatalytic —where one of the reaction products catalyzes its own formation—a circular reaction front will form around the injection point.

Stanford Scientists Cure Type 1 Diabetes in Mice Without Insulin or Immune Suppression

An “immune system reset” eliminated autoimmune, or Type 1, diabetes in mice in a study conducted at Stanford Medicine. Researchers say the strategy could also have potential for treating other autoimmune diseases and improving outcomes in organ transplantation. In a new study from Stanford Medici

Android mental health apps with 14.7M installs filled with security flaws

Several mental health mobile apps with millions of downloads on Google Play contain security vulnerabilities that could expose users’ sensitive medical information.

In one of the apps, security researchers discovered more than 85 medium-and high-severity vulnerabilities that could be exploited to compromise users’ therapy data and privacy.

Some of the products are AI companions designed to help people suffering from clinical depression, multiple forms of anxiety, panic attacks, stress, and bipolar disorder.

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