Comment

Comment by Dr. Krishna Kumari Challa on Thursday

Can't sleep? Your microbiome may play a role

Sleep is an absolute necessity but most of us aren't getting enough of it.

Sleep is required to consolidate memories, regenerate tissue and build up energy for emotional regulation and alertness during the day. Sleep deprivation disrupts these processes, increases stress and predisposes people to heart, psychiatric and neurological problems.

Factors like stress, jet lag, work, diet and screen time all interfere with our ability to get the 7–9 hours of solid slumber needed to recover from the physiological pummels of the day.

But there's more to this story than travel and cellphones. How much sleep we get, and its quality, may have ties to the microbial variety your body harbours!

We may have some control over how our sleep plays out, but many pieces of the puzzle—particularly those at the cellular level—are out of our hands. Some of them, in fact, are in our guts.
Studies in animal models and humans suggest there is a bidirectional relationship between the composition of the gut microbiota and sleep quality and duration. In mice, altering the gut microbial community, such as through antibiotic treatment, can lead to poorer, more fragmented sleep.

Comment by Dr. Krishna Kumari Challa on Thursday

Suspecting that what was changing was not the mosquitoes' ability to sense us at these times of day, but the persistence, or aggressiveness, of their response, the research team used CRISPR-Cas9, a gene editing tool, to mutate a gene that controls mosquitoes' internal clocks..
They found that mutating the gene changed their behavioral timing, making the mosquitoes less persistently responsive to carbon dioxide in the morning. Normally, biting rates are high in the mornings, but when they disrupted the clock gene, the mutant mosquitoes were less successful at feeding during that time.
This is the first time we've found that there's an internal rhythm in the mosquito's behavior that could be driving these bites at dawn and dusk. Their internal clocks make them more persistent and predatory in their response to humans at these times of day.
Scientists could, in theory, find ways to lock mosquitoes in a state that prevents them from effectively seeking out humans. This could mean fewer uncomfortable bites and less disease.
But the mosquitoes in our place bite us all the time, not only during dawn and dusk.
When we try to protect ourselves at dawn and dusk, they evolve to bite us all through the day!
Hmmm! Researchers are you listening?

Linhan Dong et al, Time-of-day modulation in mosquito response persistence to carbon dioxide is controlled by Pigment-Dispersing Factor, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2520826122

Part 2

Comment by Dr. Krishna Kumari Challa on Thursday

Could altering mosquitoes' internal clocks stop them from biting?

People who live in the tropical areas where Aedes aegypti mosquitoes reside have probably known for centuries, or even millennia—thanks to their itchy bites—that the mosquitoes hunt most often at dawn and dusk.

A new study offers scientific proof of that hunting behavior, and new insight into the biological mechanism behind it. It also offers a potential path to reducing bites and helping stop the spread of deadly, mosquito-borne disease.

The research focuses on Aedes aegypti, a type of mosquito that lives primarily in tropical areas, and that can carry diseases like dengue, chikungunya, and Zika. Although this mosquito species cannot survive harsh winters, in recent years they have made their habitats in new areas as climate change enables them to thrive in more temperate climates.

There are many reasons people could, in theory, get more bites from these mosquitoes at dawn and dusk. It could be that they're just outside more, or that humans are more attractive to them at these times. This study focused on understanding if this biting pattern is also influenced by mosquitoes' own daily rhythm.

The research team began by video recording mosquitoes, and watching how they responded to carbon dioxide, a signal mosquitoes use to locate humans. The team used machine learning to quantify the mosquitoes' movements.
They found that the mosquitoes had a more persistent response to the same amount of carbon dioxide at dawn and dusk, exactly the times of day that many people (both mosquito researchers and not) have reported getting more bites.

This is consistent with the idea that they're actually better predators at that time of day.
Part 1

Comment by Dr. Krishna Kumari Challa on Thursday

Bacteria spin rainbow-colored, sustainable textiles

In the future, clothes might come from vats of living microbes. Reporting in the journal Trends in Biotechnology, researchers demonstrate that bacteria can both create fabric and dye it in every color of the rainbow—all in one pot. The approach offers a sustainable alternative to the chemical-heavy practices used in today's textile industry.

The industry relies on petroleum-based synthetic fibers and chemicals for dyeing, which include carcinogens, heavy metals, and endocrine disruptors.

These processes generate lots of greenhouse gases, degrade water quality, and contaminate the soil, so researchers wanted to find a better solution.

Known as bacterial cellulose, fibrous networks produced by microbes during fermentation have emerged as a potential alternative to petroleum-based fibers such as polyester and nylon.

Researchers set out to create fibers with vivid natural pigment by growing cellulose-spinning bacteria alongside color-producing microbes. The microbial colors stemmed from two molecular families: violaceins—which range from green to purple—and carotenoids, which span from red to yellow.

But the first experiments failed. The team learned that the cellulose-spinning bacteria Komagataeibacter xylinus and the color-producing bacteria Escherichia coli interfered with each other's growth.

Tweaking their recipe, the researchers found a way to make peace between the microbes. For the cool-toned violaceins, they developed a delayed co-culture approach by adding in the color-producing bacteria after the cellulose bacteria had already begun growing, allowing each to do its job without thwarting the other.

For the warm-toned carotenoids, the team devised a sequential culture method, where the cellulose is first harvested and purified, then soaked in the pigment-producing cultures. Together, the two strategies yielded a vibrant palette of bacterial cellulose sheets in purple, navy, blue, green, yellow, orange, and red.

To see if the colors could survive the rigors of daily life, the team tested the materials by washing, bleaching, and heating them, as well as soaking them in acid and alkali. Most held their hues, and the violacein-based textile even outperformed synthetic dye in washing tests.

Researchers are  proposing an environmentally friendly direction toward sustainable textile dyeing while producing cellulose at the same time.

Accepting it is in your hands!

Scaling up production and competing with low-cost petroleum products are among the remaining hurdles. Real progress will also require a shift in the consumer mindset toward prioritizing sustainability over price.

But the bacteria-based fabrics are at least five years from store shelves.  

One-pot production of colored bacterial cellulose, Trends in Biotechnology (2025). DOI: 10.1016/j.tibtech.2025.09.019

Comment by Dr. Krishna Kumari Challa on Thursday

Scientists suspect that this cascade of EBV-generated self-targeting B-cell activation might extend beyond lupus to other autoimmune diseases such as multiple sclerosis, rheumatoid arthritis and Crohn's disease, where hints of EBV-initiated EBNA2 activity have been observed.
The million-dollar question: If about 95% of us are walking around with latent EBV in our B cells, why do some of us—but not all of us—get autoimmunity? The researchers speculate that perhaps only certain EBV strains spur the transformation of infected B cells into antigen-presenting "driver" cells that broadly activate huge numbers of antinuclear B cells.
Many companies are working on an EBV vaccine, and clinical trials of such a vaccine are underway. But that vaccine would have to be given soon after birth, they noted, as such vaccines are unable to rid an already-infected person of the virus.

Shady Younis et al, Epstein-Barr virus reprograms autoreactive B cells as antigen presenting cells in systemic lupus erythematosus, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.ady0210

Part 4

Comment by Dr. Krishna Kumari Challa on Thursday

But at times, somnolent autoreactive B cells become activated, take aim at our own tissues and instigate one of the disorders collectively called autoimmunity. Some awakened autoreactive B cells crank out antibodies that bind to proteins and DNA inside the nuclei of our cells. Such activated "antinuclear antibodies"—the hallmark of lupus—trigger damage to tissues randomly distributed throughout the body, because virtually all our body's cells have nuclei.

The vast majority of EBV-infected people (most of us, that is) have no idea they're still sheltering a virus and never get lupus. But essentially everyone with lupus is EBV-infected, studies have shown. An EBV-lupus connection has long been suspected but never nailed down until now.
Although latent EBV is ubiquitous in the sense that almost everybody carries it, it resides in only a tiny fraction of any given person's B cells. As a result, until the new study, it was virtually impossible for existing methods to identify infected B cells and distinguish them from uninfected ones.
But researchers now developed an extremely high-precision sequencing system that enabled them to do this. They found that fewer than 1 in 10,000 of a typical EBV-infected but otherwise healthy individual's B cells are hosting a dormant EBV viral genome.

Employing their new EBV-infected-B-cell-identifying technology along with bioinformatics and cell-culture experimentation, the researchers found out how such small numbers of infected cells can cause a powerful immune attack on one's own tissues. In lupus patients, the fraction of EBV-infected B cells rises to about 1 in 400—a 25-fold difference.
It's known that the latent EBV, despite its near-total inactivity, nonetheless occasionally nudges the B cell in which it's been snoozing to produce a single viral protein, EBNA2. The researchers showed that this protein acts as a molecular switch—in geneticists' language, a transcription factor—activating a battery of genes in the B cell's genome that had previously been at rest. At least two of the human genes switched on by EBNA2 are recipes for proteins that are, themselves, transcription factors that turn on a variety of other pro-inflammatory human genes.

The net effect of all these genetic fireworks is that the B cell becomes highly inflammatory: It dons its "professional antigen-presenting cell" uniform and starts stimulating other immune cells (called helper T cells) that happen to share a predilection for targeting cell-nuclear components. These helper T cells enlist multitudes of other antinuclear B cells as well as antinuclear killer T cells, vicious attack dogs of the immune system.

When that militia bulks up, it doesn't matter whether any of the newly recruited antinuclear B cells are EBV-infected or not. (The vast majority of them aren't.) If there are enough of them, the result is a bout of lupus.
Part 3

Comment by Dr. Krishna Kumari Challa on Thursday

Once you've been infected by EBV, you can't get rid of it, even if you remain or become symptom-free. EBV belongs to a large family of viruses, including those responsible for chickenpox and herpes, that can deposit their genetic material into the nuclei of infected cells. There the virus slumbers in a latent form, hiding from the immune system's surveillance agents. This may last as long as the cell it's hiding in stays alive; or under certain conditions, the virus may reactivate and force the infected cell's replicative machinery to produce myriad copies of themselves that break out to infect other cells and other people.
Among the cell types in which EBV takes up permanent residence are B cells, immune cells that do a couple of important things after they ingest bits of microbial pathogens. For one, they can produce antibodies: customized proteins that find and bind immune-system-arousing proteins or other molecules (immunologists call them "antigens") on microbial pathogens that have infected an individual, or are trying to.

In addition, B cells are what immunologists call "professional antigen-presenting cells": They can process antigens and display them on their surfaces in a way that encourages other immune cells to raise the intensity of their hunt for the pathogen in question. That's a substantial force multiplier for kick-starting an immune response.

Our bodies harbor hundreds of billions of B cells, which over the course of numerous rounds of cell division develop an enormous diversity of antibodies. In the aggregate, these antibodies can bind an estimated 10 billion to 100 billion different antigenic shapes. This is why we're able to mount a successful immune response to so many different pathogens.

Oddly, about 20% of the B cells in our bodies are autoreactive. They target antigens belonging to our own tissues—not by design, but due to the random way B-cell diversity comes about: through sloppy replication, apparently engineered by evolution to ensure diversification. Fortunately, these B cells are typically in a dopey state of inertia, and they pretty much leave our tissues alone.
Part 2

Comment by Dr. Krishna Kumari Challa on Thursday

Scientists tie lupus to a virus nearly all of us carry

One of humanity's most ubiquitous infectious pathogens bears the blame for the chronic autoimmune condition called systemic lupus erythematosus (lupus), Stanford Medicine investigators and their colleagues have found.

The Epstein-Barr virus (EBV), which usually resides silently inside the bodies of 19 out of 20 people, is directly responsible for commandeering what starts out as a minuscule number of immune cells to go rogue and persuade far more of their fellow immune cells to launch a widespread assault on the body's tissues, the scientists have shown.

The work is published in the journal Science Translational Medicine.

About five million people worldwide have lupus, in which the immune system attacks the contents of cell nuclei. This results in damage to organs and tissues throughout the body—skin, joints, kidneys, heart, nerves and elsewhere—with symptoms varying widely among individuals. For unknown reasons, nine out of 10 lupus patients are women.

With appropriate diagnosis and medication, most lupus patients can live reasonably normal lives, but for about 5% of them the disorder can be life-threatening. 

Existing treatments slow down disease progression but don't 'cure' it.

By the time we've reached adulthood, the vast majority of us have been infected by EBV. Transmitted in saliva, EBV infection typically occurs in childhood, from sharing a spoon with or drinking from the same glass as a sibling or a friend, or maybe during our teen years, from exchanging a kiss. EBV can cause mononucleosis, "the kissing disease," which begins with a fever that subsides but lapses into a profound fatigue that can persist for months.

Practically the only way to not get EBV is to live in a bubble. If you've lived a normal life the odds are nearly 20 to 1 you've got it.

part 1

Comment by Dr. Krishna Kumari Challa on Thursday

Selecting for low activity successfully caused slower movement across the four generations. The researchers analyzed the composition of the microbial community and found that this reduction in activity was linked to higher levels of the bacterium Lactobacillus, which produces the substance indolelactic acid (ILA). They also showed the link was causal. When they independently gave Lactobacillus or ILA to other mice, it was enough to suppress their locomotion.

This work highlights the role of microbiome-mediated trait inheritance in shaping host ecology and evolution," wrote the researchers in a paper.

The novelty in our study lies in experimentally demonstrating that selection on a host trait can lead to changes in that same trait over time purely through microbiome transmission, without any genetic evolution in the host.

 Taichi A. Suzuki et al, Selection and transmission of the gut microbiome alone can shift mammalian behavior, Nature Communications (2025). DOI: 10.1038/s41467-025-65368-w

Part 2

Comment by Dr. Krishna Kumari Challa on Thursday

Gut microbes pass down behavioral traits in mice offspring independent of genes

Gut microbes are essential partners that help digest food, produce vitamins and train the immune system. They can also pass on behavioral traits to their host's offspring, at least in mice. Scientists have discovered that the mouse microbiome can alter the animal's behaviour in just four generations, independent of its genes. The study is published in the journal Nature Communications

Animals and their microbes have coevolved for millions of years. While it was already known that bacteria, viruses and fungi living in the gut can drive inherited changes in some simple creatures, like insects, scientists didn't know till now whether they could be the sole mechanism for passing down a specific trait (like a behavioral tendency) in more complex animals, such as mammals.

The research team designed an experiment in which they strictly controlled the host animal's genes. First, they took gut microbiota from wild-derived mice and gave it to genetically identical germ-free mice in the lab.
Then they set up a selection line, repeatedly choosing the two mice that traveled the least and transferring their microbes into a fresh batch of genetically identical, germ-free mice for the next generation. The scientists focused on locomotor activity (movement) because previous tests had confirmed that it was a behavior strongly influenced by the microbiome. The researchers also ran a control line where two donor mice were chosen at random.

This serial transfer of gut microbes carried on for four generations. By using germ-free mice, the researchers could be sure that any behavioral changes they observed were due to the selection and transfer of the microbial community.
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