Top story:  “Antidepressants:  A new weapon against allergies?”

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Accessed on 13 September 2023, 1809 UTC.

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13th September, 2023
Today’s Protostar is Bruna Araujo David, who helped uncover how diseased livers keep fighting infections. But first, catch up on the latest science news, including evidence that cannabinoids help mice see the joy in life and how chemo can accidentally awaken cancerous cells.
Fighting allergies with antidepressants
Antidepressant drugs known as selective serotonin reuptake inhibitors (SSRIs) provide welcome relief for many patients suffering from depression and anxiety. These medications work by increasing the amount of serotonin—a neurotransmitter that, among other functions, helps regulate mood and sleep—in the brain. But SSRIs may have an unexpected secondary effect: According to new research, they’re really good at treating allergic reactions.

Now, in Science Signaling, scientists report that fluoxetine—an SSRI better known as Prozac—effectively reduces symptoms of allergic inflammation in mice. The drug works by suppressing a type of immune cell known as mast cells, which play a prominent role in allergic reactions. When allergens bind to receptors on the surface of mast cells, they respond by vomiting a slew of inflammatory compounds into the bloodstream. These compounds can sometimes cause a severe, potentially fatal condition called anaphylaxis. One of the most dangerous symptoms of anaphylaxis is throat swelling, which can block a patient’s airway and make it impossible for them to breathe.

The researchers found that fluoxetine was able to inhibit the function of mast cells, reducing airway inflammation and other symptoms of anaphylaxis in mouse models. Since SSRIs are already widely prescribed and have been shown to be relatively safe, the study authors believe that the drug could be conveniently repurposed to treat patients with allergic diseases.

Miserable mice get a lift from innate cannabis-like compounds
Molecularly speaking, the THC that makes cannabis an appealing recreational drug is a cannabinoid. Our brains produce similar molecules, and a new study in mice suggests that the release of cannabinoids by a part of the brain called the amygdala plays a key role in relieving stress and enabling them to experience the joy of life.

The research, published yesterday in Cell Reports , employed a new protein sensor that detects cannabinoids in real time to probe how they function in the brains of mice. Several different kinds of stress led to the release of cannabinoids by the amygdala, the team observed. And this played an important role in destressing: When the team removed the protein that compounds interact with, the mice became downright pitiful. They just didn’t want to move after stressful events and showed little interest in a sweet drink that healthy mice find divine. This kind of blasé reaction to what should be a wonderful thing indicates a general lack of feeling pleasure—what psychologists call anhedonia—often seen in people with stress-related mental health conditions like post-traumatic stress disorder.

“Determining whether increasing levels of endogenous cannabinoids can be used as potential therapeutics for stress-related disorders is a next logical step from this study and our previous work,” says coauthor and Northwestern University psychiatrist Sachi Patel in a press release.

Chemo accidentally awakens sleeping breast cancer
When breast cancer is discovered, swift treatment can often knock it into remission. But nearly one-quarter of breast cancers come back within five years. Understanding how and why cancer recurs could help oncologists predict or prevent it. Now, a new study suggests the very drugs that knock the cancer down in the first place could be partly to blame.

In an ideal world, chemotherapy drugs would kill cancerous cells without causing any harm to healthy ones. But in reality, they just hurt cancer cells more, and sometimes those cells can escape the toxic effects by going dormant. If such sleeping cells reawaken, a person’s cancer recurs. And that’s exactly what researchers found can happen with the common cancer drug known as docetaxel: Experiments in cultured cells and mice revealed that healthy cells harmed by the drug release signaling molecules that wake up dormant cancer cells.

On the upside, antibodies designed to glom onto those signaling molecules kept the cancerous cells from growing and dividing again. That means the right companion drugs could allow patients to receive the benefits of chemo without this drawback, the researchers say.

Changing the brain game
Changing the brain game
The exquisite complexity of the brain has hamstrung efforts to develop effective treatments for neurodegenerative diseases. This Science Webinar will explore how organoids, assembloids, and stem cells are driving progress toward treatments.
Bruna Araujo David
Bruna Araujo David
Postdoctoral research fellow, University of Calgary

Pieseler, M et al. Kupffer cell–like syncytia replenish resident macrophage function in the fibrotic liver. Science 381 (2023). 10.1126/science.abq5202

Bruna Araujo David says her career in science started “late.” Raised by a single mom in what she describes as a low-income household in Brazil, she was the first in the family to have a post-secondary degree. While she always liked biology, she thought she might become a teacher, not a scientist. Growing up, she associated science and research with the men wearing white coats she saw occasionally on news broadcasts. Things started to change in her last year of college when she somewhat serendipitously joined the lab of Gustavo Menezes, whose research focused on the liver. “My whole life trajectory changed just like that,” she recalls. She ended up staying in the lab for her master’s and Ph.D. “I’ve been studying the liver ever since.”

Indeed, as a postdoctoral researcher in Paul Kubes’ lab at the University of Calgary, she worked alongside fellow postdoc and clinician scientist Moritz Peiseler to understand how livers that become rife with scar tissue—a condition known as fibrosis, which occurs in many liver diseases—are still able to battle blood-borne pathogens. In doing so, she earned co-first authorship on the recent Science paper reporting their findings: that when a liver becomes fibrotic, its huge, resident bacteria-eating immune cells—macrophages called Kupffer cells—get a kind of cellular amnesia and forget what they’re supposed to do. Luckily, macrophages from elsewhere in the body come to the rescue, forming ‘superclusters’ that take over the job of filtering bacteria from the blood.

ScienceAdviser recently talked with David about the work. Below is that conversation, edited for brevity.

How did you end up working on this particular project?
That was a project Moritz started. He wanted to better understand the fibrotic liver, because it’s something he sees a lot in the clinic. And the immune component of liver fibrosis, it’s overlooked. The basic biology of it—and I kind of hate the word basic here, because it gives the impression that it’s not important—but the basic, or perhaps foundational biology, was not well explored. And he ended up finding these giant macrophage clusters that no one had ever seen before, and that’s when the project took shape and we began to investigate the origin of them, which is a huge part of the paper.

In addition to the big cells, we found these huge morphological changes in the liver, which was something we were not expecting. Also, people had assumed that the liver’s immune cells were dying and disappearing in fibrosis. But that was because of how people usually visualize them: using proteins on the surface of them that they can label. But [when the liver becomes fibrotic,] those are not there anymore; they are downregulated. The macrophages are still there, they’ve just lost their identity. I think one of the reasons we were able to find everything we did was because we did a lot of in vivo imaging.

And one of the things you found was that even though these Kupffer cells stop functioning, the liver has a backup system of sorts, right?
Exactly. The fascinating adaptability of the liver is something I’m continually amazed by. I’ve been working with the liver for so long, but that was still surprising.

Now, this was in a mouse model. Would you say there are clinical implications?
Well, we saw a very similar phenomenon in humans. The question becomes: With all the information we have now, how can we help mice and potentially humans overcome this whole architecture change of the liver? How can we potentially use what we’ve learned to help with infections and liver function? I think the findings so far don’t necessarily give us the answer, but we definitely have more information now about what’s going on. Now the knowledge can move forward and eventually get to a therapy or something more clinically related.

What’s next for you?
I’m working on another project, which is my baby. It has been my main project for a while. It’s also, of course, liver-related. But it’s focused on understanding how the liver and the same macrophage population play a role in neonatal infections. We already know that the cells don’t work as well as in adults. Now we are investigating why, to understand why babies are way more susceptible to infections—and these macrophages in the liver play a big role in that susceptibility. And hopefully we can use that [information] to better deal with newborn and neonatal infection, which is a huge problem.

I think it’s very important to highlight how these foundational blocks of knowledge are important. Because I feel like people in general, they rush to get to the clinic and unfortunately, sometimes things don’t work because we don’t have the knowledge we need first. People have to have patience.

Why, it’s (not) greased lightning!
The brief flashes of light that occasionally illuminate the atmosphere of Venus might be meteors, not lightning, which is good news for future probes.
High-risk, high-reward
The U.K.’s Advanced Research & Invention Agency has announced eight program directors, each of whom will provide up to £50 million in funding for “high-risk, high-reward” research.
Are you sitting comfortably?
Older adults who spend a lot of time engaging in sedentary behaviors may be more likely to develop dementia.
Watchdog finds forever home
In return for stable funding, the influential website and database Retraction Watch is teaming up with Crossref.
The United States needs to rethink its entire innovation ecosystem to incorporate equity as a foundational guiding principle…
Last but not least
The story of what went on behind closed doors in the CIA regarding the origins of SARS-CoV-2 has another twist, and it’s a doozy.
Christie Wilcox, editor, ScienceAdviser

With contributions from Phie Jacobs

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