Astrophysicists Discover Long-sought Energetic Hot Wind from Low-luminosity Active Galactic Nucleus (Planetary Science)

Supermassive black holes in the universe are swallowing gas round them. The infalling gas is called black hole accretion flow. In a study published in Nature Astronomy, the group led by Prof. YUAN Feng at Shanghai Astronomical Observatory (SHAO) of the Chinese Academy of Sciences, together with the group led by Prof. LI Zhiyuan at Nanjing University, found direct evidence for the existence of an energetic hot wind launched from the hot accretion flow onto a weakly accreting supermassive black hole, representing a step toward understanding accretion processes around black hole.

There exists a supermassive black hole in almost every galaxy in the universe. The gas round the black hole will be accreted and form an accretion disk. Strong radiation is emitted from the accretion disk, which is the origin of the radiation in the first image of black holes people have obtained in 2019.

Depending on the gas temperature, black hole accretion flows are divided into two types, namely cold and hot ones. Theoretical studies performed by the SHAO group over the past ten years predicted that strong wind must exist in hot accretion flows that typically feed low-luminosity active galactic nuclei (LLAGN). These winds are also found to play a crucial role in galaxy evolution, according to the state-of-the-art cosmological simulation Illustris-TNG. However, direct observational evidence for such a wind proved difficult to obtain.

The researchers in this study found strong observational evidence for an energetic outflow from M81*, a prototype LLAGN residing in the nearby massive spiral galaxy Messier 81 by analyzing a high-quality X-ray spectrum. The spectrum, which has unparalleled resolution and sensitivity, was taken by the Chandra X-ray Observatory in the years of 2005-2006, but remained unexplored for the wind aspect until now.

The outflow from M81* is evidenced by a pair of Fe XXVI Lyα emission lines that quasi-symmetrically redshifted and blueshifted at a bulk line-of-sight velocity of 2800 kilometer per second, and a high Fe XXVI Lyα-to-Fe XXV Kα line ratio that implies a temperature of 140 million degree of Kelvin of the line-emitting plasma.

To interpret the high-velocity and high-temperature plasma, the researchers carried out magnetohydrodynamic simulations of the hot accretion flow onto M81* and produced synthetic X-ray spectrum of the wind launched from the hot accretion flow as predicted by the numerical simulations. The predicted emission lines were in agreement with the Chandra spectrum, providing evidence for the existence of a hot wind. Energetics of this wind was found to be sufficiently strong to affect the close environment of M81*.

This study revealed the missing link between observations and the theory of hot accretion flows, as well as the latest cosmological simulations with AGN feedback.

Reference: Shi, F., Li, Z., Yuan, F. et al. An energetic hot wind from the low-luminosity active galactic nucleus M81*. Nat Astron (2021).

Provided by Chinese Academy of Sciences

First Measurement Of Isotopes in Atmosphere Of Exoplanet (Planetary Science)

An international team of astronomers have become the first in the world to detect isotopes in the atmosphere of an exoplanet. It concerns different forms of carbon in the gaseous giant planet TYC 8998-760-1 b at a distance of 300 light years in the constellation Musca (Fly). The weak signal was measured with ESO’s Very Large Telescope in Chile and seems to indicate that the planet is relatively rich in carbon-13. The astronomers speculate that this is because the planet formed at a great distance from its parent star. The research will be published in the scientific journal Nature on Thursday.

Isotopes are different forms of the same atom, but with varying number of neutrons in the nucleus. For example, carbon with six protons typically has six neutrons (carbon-12), but occasionally seven (carbon-13) or eight (carbon-14). This does not change much the chemical properties of carbon, but isotopes are formed in different ways and often react slightly differently to the prevailing conditions. Isotopes are therefore used in a wide range of research fields: from detecting cardiovascular disease or cancer to studying climate change and determining the age of fossils and rocks.

Quite special

The astronomers were able to distinguish carbon-13 from carbon-12 because it absorbs radiation at slightly different colours. “It is really quite special that we can measure this in an exoplanet atmosphere, at such a large distance,” says Leiden PhD student Yapeng Zhang, first author of the article.

The astronomers had expected to detect about one in 70 carbon atoms to be carbon-13, but for this planet it seems to be twice as much. The idea is that the higher carbon-13 is somehow related to the formation of the exoplanet.

Co-author Paul Mollière, from the Max Planck Institute for Astronomy in Heidelberg, Germany, explains:  “The planet is more than one hundred and fifty times further away from its parent star than our Earth is from our Sun. At such a great distance, ices have possibly formed with more carbon-13, causing the higher fraction of this isotope in the planet’s atmosphere today.”

Story continues below animation of isotopes on exoplanets.

‘My exoplanet’

The planet itself, TYC 8998-760-1 b, was discovered only two years ago by Leiden PhD student Alexander Bohn, co-author of the article. “It’ s awesome that this discovery has been made close to ‘my’ planet. It will probably be the first of many.”

Ignas Snellen, professor in Leiden and for many years the driving force behind this subject, is above all proud. “The expectation is that in the future isotopes will further help to understand exactly how, where and when planets form. This is just the beginning.”

Featured image: Cartoon about the discovery of carbon-13 in the atmosphere of an exoplanet. In reality, the astronomers were sitting behind their desks analysing the spectra of the exoplanet TYC-8998 b made by ESO’s Very Large Telescope in Chile. (c) Daniëlle Futselaar (Artsource)

Scientific paper
The 13CO-rich atmosphere of a young accreting super-Jupiter. By: Yapeng Zhang, Ignas A.G. Snellen, Alexander J. Bohn, Paul Mollière, Christian Ginski, H. Jens Hoeijmakers, Matthew A. Kenworthy, Eric E. Mamajek, Tiffany Meshkat, Maddalena Reggiani, Frans Snik. Nature, 15 July 2021. [original | preprint (pdf)]

Provided by NOVA

Scientists Identify New Gut–liver Drug Recycling Process (Medicine)

Implications for Developing Treatments for Intestinal Diseases

A team of University of Houston pharmaceutical researchers is reporting a newly recognized process of drug metabolism in the intestines – followed by recycling through the liver – that could have important implications for developing treatments for intestinal diseases and for taking multiple medications at the same time. 

“The intestines play a crucial role in metabolizing and recycling certain plant compounds and drugs,” reports Ming Hu, Diana S-L. Chow Endowed Professor of Drug Discovery and Development at the UH College of Pharmacy and the senior author of the paper in eLife. “The discovery has important implications for scientists trying to understand how both phytochemicals (a type of plant compound, such as flavonoids) and medicines are metabolized in the body.” 

The new information could help chemists develop better drugs and clinicians to fine-tune medication dosing, especially when dealing with polypharmacy, where a patient takes multiple drugs at the same time. 

Ming Hu, Diana S-L. Chow Endowed Professor of Drug Discovery and Development at the UH College of Pharmacy
Ming Hu, Diana S-L. Chow Endowed Professor of Drug Discovery and Development at the UH College of Pharmacy, reports a newly recognized process of drug metabolism in the intestines. © University of Houston

Scientists have long recognized that bile acid is produced in the liver and released into the intestines and is then recycled back through the liver for reuse as the bile. Some medications that are metabolized in the liver also go through this process, known as enterohepatic recycling (EHR). This can extend the life of drugs in the body, which may affect how well they work and whether they cause side effects. 

“The liver has long been considered the most important organ for drug metabolism,” said lead author Yifan Tu, who conducted the study while he was doing his doctoral work at the UH College of Pharmacy.  “But we’ve shown that the intestines also play a major role in drug metabolism.” 

In their experiments, the team administered 16 different types of flavonoids or drugs directly to the liver or intestines and then tracked what happened to the treatments. They found that some drugs and compounds were metabolized in the intestines and the metabolites were then transported to the liver before being cycled back into the intestines.  

“In this process, the liver acts only as a recycling organ, which is rare, since the liver is known to be the metabolic ‘superstar’ organ in humans,” said Tu, who is now a postdoctoral fellow at the pharmaceutical company Boehringer Ingelheim in Connecticut.  

The team has called this new mechanism ‘hepatic enteric recycling’ (HER). They found that, in this process, the roles of the liver and intestines are reversed. “This may explain why some drugs or plant compounds have larger effects on the intestine than anticipated and could help scientists understand how intestinal diseases may alter drug metabolism in the body,” said Tu. 

“We hope our findings will be useful for medicinal chemists to design new drugs tailored to treat intestinal, especially colonic diseases,” said Hu.

Featured image: The intestines play a crucial role in metabolizing and recycling certain plant compounds and drugs. © University of Houston

Reference: Yifan Tu et al., “Hepatoenteric recycling is a new disposition mechanism for orally administered phenolic drugs and phytochemicals in rats”, elife, 2021. DOI: 10.7554/eLife.58820

Provided by University of Houston

Researchers Identified Small Molecule Inhibitor That Reduces The Growth Of Uveal Melanoma (Medicine)

A small molecule inhibitor has been identified that reduces the growth of uveal melanoma, a rare and deadly cancer of the eye.

Uveal melanoma, or UM, is a rare and deadly cancer of the eye, and the mortality rate has remained unimproved for 40 years. Half of the melanomas spread to other organs of the body, causing death in less than a year, so new treatments to preserve vision and prevent death are an urgent need.  

Now a preclinical study by researchers at the University of Alabama at Birmingham and Emory University, Atlanta, offers hope — a small molecule inhibitor has been identified that dampens the potent drivers of this tumor. In mouse models, the inhibitor, KCN1, strongly limited primary disease in the eye and metastatic tumor dissemination to the liver, and animals survived longer, without overt side effects.

Thus, this class of inhibitory compounds shows promise, though the co-leaders of the research — Erwin Van Meir, Ph.D., professor of neurosurgery at UAB, and Hans Grossniklaus, M.D., MBA, professor of ophthalmic pathology at Emory — say the drug needs further optimization before clinical use. 

“Overall,” they wrote in the paper published in the journal Oncogene, “our preclinical studies support the further translation of the KCN1 arylsulfonamide scaffold toward a novel treatment for patients with metastatic uveal melanoma.” The uvea is the pigmented layer of the eye.

Prior to this study, it was known that: 1) a hypoxia gene signature, indicative of low oxygen levels in the tumor, is associated with poor prognosis and a high metastatic rate in uveal melanoma; 2) the hypoxia-inducible transcription factor, or HIF, turns on a large number of gene products with critical roles in cancer growth and metastasis; and 3) for UM specifically, HIF promotes tumor progression by regulating proliferation, migration, invasion and adhesion of tumor cells, as well as promoting blood vessel growth to feed the tumor. 

Dr. Erwin Van Meir headshot
Erwin Van Meir, Ph.D., professor of neurosurgery at UAB (Photo by: Lexi Coon)

Little was known of the role of HIF in directing pro-invasive extracellular matrix remodeling in UM. Changes in the extracellular matrix, including increased collagen deposition and reorganization of collagen fibers outside the cell, is known to aid cancer progression and tumor cell invasion. Extracellular matrix is the non-cellular component of all tissues that provides physical scaffolding for cells and has other biochemical roles.

Hypoxia promotes collagen deposition, in part, because HIF increases production of two gene products, P4HA1 and P4HA2, that are part of an enzyme complex that adds hydroxyl residues to prolines in procollagen. Procollagen is a precursor protein in the complex maturation process that collagen undergoes.

In their study, Van Meir, Grossniklaus and colleagues decided to evaluate the expression of the P4HA1/2 genes in relation to UM patient prognosis, and to determine whether inhibiting hypoxia-induced P4HA1/2 expression in a preclinical model of metastatic UM would yield therapeutic benefit.

They found that P4HA1 and P4HA2 were induced by hypoxia in human UM cell lines, and this induction was reduced by KCN1. Comparison of 46 patients with non-metastatic UM and 46 with metastatic UM showed that P4HA1/2 were significantly overexpressed in patients with metastatic disease. Also, P4HA1/2 expression correlated with poor overall survival in UM patients. This suggests that P4HA1 and P4HA2 can serve as prognostic markers in UM, and that they may be important for malignant progression of the disease and patient survival.

The researchers next turned to preclinical animal models of UM. They showed that KCN1 was abundantly taken up in the liver and the eyes after intraperitoneal injection, and it dampened tumor growth and disease burden at the primary site of the eye, as well as reduced distant metastases in the liver. KCN1 also increased survival in three different models that test the growth of human UM after injection in mice uvea. The inhibitor was most effective at reducing metastases when it was administered early.

At the molecular level, treatment with KCN1 to inhibit the hypoxic induction of P4HA1/2 decreased the hydroxylation of proline amino acids in the procollagen. It also caused cleavage of the collagen and disordered the structure of collagen VI, a mature structural component of the extracellular matrix. These collagen changes correlated with a reduction in tumor cell invasion.

“Our study,” Van Meir and Grossniklaus concluded, “suggests that KCN1 has desirable properties as a suppressor of metastasis: It is well tolerated, has excellent distribution to the eye and the liver, and is thus ideally suited for treating metastatic UM.”

Co-first authors of the report, “Targeting HIF-activated collagen prolyl 4-hydroxylase expression disrupts collagen deposition and blocks primary and metastatic uveal melanoma growth,” are Stefan Kaluz and Qing Zhang, Emory University. Additional co-authors are Yuki Kuranaga and Satoru Osuka, UAB Department of Neurosurgery; Hua Yang, Debanjan Bhattacharya, Narra S. Devi, Jiyoung Mun and Mark M. Goodman, Emory University; and Wei Wang and Ruiwen Zhang, University of Houston. 

Support came from National Institutes of Health grants CA116804, CA176001, CA180805, EY017045, EY06360, CA138292 and CA13148; and National Natural Science Foundation of China grant NNS81201808. Support also was provided by a Fight For Sight Postdoctoral Award, the Emory Melanoma Prevention and Research Discovery Fund, a Winship Cancer Institute pilot grant, a Central South University Lieying pilot grant, the V Foundation, the Max Cure Foundation, the Samuel Waxman Cancer Research Foundation, the Alan B. Slifka Foundation, and Research to Prevent Blindness, Inc. 

Van Meir came to UAB from Emory in fall 2019, and he is the associate director for Shared Resources at the O’Neal Comprehensive Cancer Center at UAB.

Provided by UAB

Floating Into Summer With More Buoyant, Liquid-proof Life Jackets, Swimsuits (Chemistry)

Summertime is here, and that often means long, lazy days at the beach, water skiing and swimming. Life jackets and swimsuits are essential gear for these activities, but if not dried thoroughly, they can develop a gross, musty smell. Now, researchers reporting in ACS Applied Materials & Interfaces have developed a one-step method to create a buoyant cotton fabric for these applications that is also oil- and water-repellant. 

Waterproof and oil-proof fabrics are in high demand for recreational water activities because of their low drag and self-cleaning properties. And while cotton is a popular fabric, it’s hydrophilic, so most liquids and dirt can easily mess it up. To improve cotton’s impermeability, previous researchers developed superamphiphobic coatings that were extremely water- and oil-repellant. But because they required multiple time-consuming steps to apply, these coatings were impractical for large-scale manufacturing. Others incorporated nanoparticles into their formulas, but there are concerns about these particles sloughing off and potentially harming the environment. Xiao Gong and Xinting Han wanted to develop a simple way to make a coating for cotton fabric so it would have superb liquid-repulsion properties and hold up in many challenging circumstances.

The researchers optimized a one-step process for a liquid-proof coating by mixing dopamine hydrochloride, 3-aminopropyltriethoxysilane and 1H,1H,2H,2H-perfluorodecyltriethoxysilane with a piece of cotton fabric for 24 hours. The three-part solution developed into a uniform, dark brown coating on the fabric. In tests, the treated cotton was impervious to many common liquids. The new solution also coated inner cotton fibers, making them liquid proof, too. In other tests, only strong acid and repeated washings reduced the material’s water and oil resistance, respectively. Treated fabric soiled with fine sand was easy to clean with water, whereas water only wetted the control version. Finally, the material stayed afloat with up to 35 times its weight on it because of nanoscale air pockets that formed where the coating attached to the fabric, the researchers explain. They say their durable cotton fabric has great potential for applications where drag reduction and increased buoyancy are important, including swimsuits and life jackets. 

The authors acknowledge funding from the National Natural Science Foundation of China and the Opening Project of State Key Laboratory of Polymer Materials Engineering (Sichuan University).

Reference: “In Situ, One-Pot Method to Prepare Robust Superamphiphobic Cotton Fabrics for High Buoyancy and Good Antifouling”
ACS Applied Materials & Interfaces

Provided by ACS

New Spray Could Someday Help Heal Damage After A Heart Attack (Medicine)

Many survivors of heart attacks experience long-term effects, but a new spray could someday help heal this tissue damage.

Heart attack, or myocardial infarction, is one of the leading causes of death worldwide. Although modern surgical techniques, diagnostics and medications have greatly improved early survival from these events, many patients struggle with the long-term effects of permanently damaged tissue, and the 5-year mortality rate remains high. Now, researchers reporting in ACS Nano have developed a minimally invasive exosome spray that helped repair rat hearts after myocardial infarction.

Scientists have explored using stem cell therapy as a way to regrow tissue after a heart attack. But introducing stem cells directly to the heart can be risky because they could trigger an immune response or grow uncontrollably, resulting in a tumor. Therefore, researchers have tried injecting exosomes –– membrane-bound sacs containing proteins, lipids and nucleic acids secreted by stem cells ––  into the heart, but they often break down before they can have therapeutic effects. Others have developed cardiac patches, or scaffolds that help implanted exosomes last longer, but they usually must be placed on the heart during open-chest surgery. Yafeng Zhou and colleagues wanted to develop an exosome solution that could be sprayed onto the heart through a tiny incision, avoiding major surgery.

The researchers mixed exosomes from mesenchymal stem cells with fibrinogen, a protein involved in blood clotting. They added this solution to a tiny, double-barreled syringe that contained a separate solution of another clotting protein called thrombin. When the team sprayed the solutions out of the syringe onto a rat’s heart through a small chest incision, the liquids mixed and formed an exosome-containing gel that stuck to the heart. A mini-endoscope, inserted through a second small incision, guided the spray needle. In rats that had recently had a heart attack, the exosome spray lasted longer, healed injuries better and boosted the expression of beneficial proteins more than heart-injected exosomes. In pigs, the spray caused less severe immune reactions and surgical stress than open-chest surgery. The spray is a promising strategy to deliver therapeutic exosomes for heart repair, the researchers say.

The authors acknowledge funding from the National Natural Science Foundation of China and the Natural Scientific Fund of Jiangsu province.

“A Minimally Invasive Exosome Spray Repairs Heart after Myocardial Infarction”
ACS Nano

Featured image Credit: Orawan Pattarawimonchai/

Provided by ACS

Like Priming A Pump, Changes in Cells Damaged By Chronic Lung Disease Can Result in Severe COVID-19 (Medicine)

Results from a TGen-led international study suggest that SARS-CoV-2 takes advantage of genetic changes among patients with pre-existing lung diseases

The results of a study by an international scientific team co-led by the Translational Genomics Research Institute (TGen), an affiliate of City of Hope, suggest that — like pouring water atop a wellhead before pumping — the airway cells of patients with chronic lung diseases are “primed” for infection by the COVID-19 virus, resulting in more severe symptoms, poorer outcomes and a greater likelihood of death.

The study — published today in Nature Communications — details the genetic changes caused by chronic lung disease in the molecular makeup of a variety of cells, including the epithelial cells that line the lung and airways. The study details how those changes can help enable SARS-CoV-2, the virus that causes COVID-19, to enter the body, replicate and trigger an out-of-control immune response that fills the lungs with fluids and often results in patients needing respirators and lengthy hospitalizations.

The team used single-cell RNA sequencing technology to spell out the genetic code of 611,398 cells from various data bases, representing those with both healthy (control) lungs and those with chronic lung disease. Sequencing and analysis allowed researchers to identify molecular characteristics that may account for worse COVID-19 outcomes.

“Our results suggest that patients with chronic lung disease are molecularly primed to be more susceptible to infection by SARS-CoV-2,” said Nicholas Banovich, Ph.D., an Associate Professor in TGen’s Integrated Cancer Genomics Division, and one of the study’s senior authors. Dr. Banovich is a leading participant in the Human Cell Atlas Lung Biological Network, whose dozens of members, representing more than 80 institutions worldwide, also contributed to this study.

In addition, older-age, male-gender, smoking, and co-morbidities such as high blood pressure, obesity  and diabetes, are all COVID-19 risk factors that are exacerbated by chronic lung diseases, such as Chronic Obstructive Pulmonary Disease (COPD), Interstitial Lung Disease (ILD), and especially Idiopathic Pulmonary Fibrosis (IPF), a progressive scaring and stiffening of the lung tissue.

“It was recognized early in the pandemic that patients with chronic lung diseases were at particularly high risk for severe COVID-19, and our goal was to gain insight into the cellular and molecular changes responsible for this,” said Jonathan Kropski, M.D., Associate Professor of Medicine and Cell and Developmental Biology at Vanderbilt University Medical Center, and a co-senior author of the study.

Changes in lung cells and immune cells

Researchers specifically searched for changes in AT2 cells, a major lung epithelial cell type, focusing on cellular pathways and expression levels of genes associated with COVID-19. They established a “viral entry score,” a composite of all genes associated with SARS-CoV-2, and found higher scores among cells from patients with chronic lung disease.

They also explored changes in immune cells and discovered dysregulated gene expression associated with hyper-inflammation and with sustained cytokine production, two signature symptoms of severe SARS-CoV-2 infection. So-called cytokine storms in COVID-19 patients unleash a cascade of immune cells that flood the lungs, causing severe organ damage.

“The genetic changes in immune cells, especially in specialized white blood cells known as T cells, may diminish the patient’s immune response to viral infection and lead to higher risk of severe disease and poor outcomes in patients with chronic lung disease,” said Linh Bui, Ph.D., a post-doctoral fellow in Dr. Banovich’s lab, and one of the study’s lead authors.

“Our data suggest that the immune microenvironment at both the molecular and cellular levels in lungs damaged by chronic diseases may promote severe COVID-19,” Dr. Bui said. 

Significant contributions to this study were made by: Vanderbilt University Medical Center, Yale School of Medicine, Harvard Medical School, Baylor College of Medicine, and the Department of Veterans Affairs Medical Center. Plus several institutes in the UK, including: London’s Imperial College, Royal Brompton and Harefield National Health System Foundation Trust, Edinburgh University Medical School, and the Royal Infirmary of Edinburgh.

Major funding for this study — Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity — was provided by the National Institutes of Health, the Department of Defense, the Department of Veterans Affairs, and the Doris Duke Charitable Foundation.

Reference: Bui, L.T., Winters, N.I., Chung, MI. et al. Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity. Nat Commun 12, 4314 (2021).

Provided by Tgen

Trust Me, I’m A Chatbot (Business)

Göttingen University researchers investigate effect of non-human conversation partners in customer services

More and more companies are using chatbots in customer services. Due to advances in artificial intelligence and natural language processing, chatbots are often indistinguishable from humans when it comes to communication. But should companies let their customers know that they are communicating with machines and not with humans? Researchers at the University of Göttingen investigated. Their research found that consumers tend to react negatively when they learn that the person they are talking to is, in fact, a chatbot. However, if the chatbot makes mistakes and cannot solve a customer’s problem, the disclosure triggers a positive reaction. The results of the study were published in the Journal of Service Management.

Previous studies have shown that consumers have a negative reaction when they learn that they are communicating with chatbots – it seems that consumers are inherently averse to the technology. In two experimental studies, the Göttingen University team investigated whether this is always the case. Each study had 200 participants, each of whom was put into the scenario where they had to contact their energy provider via online chat to update their address on their electricity contract following a move. In the chat, they encountered a chatbot – but only half of them were informed that they were chatting online with a non-human contact. The first study investigated the impact of making this disclosure depending on how important the customer perceives the resolution of their service query to be. In a second study, the team investigated the impact of making this disclosure depending on whether the chatbot was able to resolve the customer’s query or not. To investigate the effects, the team used statistical analyses such as covariance and mediation analysis.

The result: most noticeably, if service issues are perceived as particularly important or critical, there is a negative reaction when it is revealed that the conversation partner is a chatbot. This scenario weakens customer trust. Interestingly, however, the results also show that disclosing that the contact was a chatbot leads to positive customer reactions in cases where the chatbot cannot resolve the customer’s issue. “If their issue isn’t resolved, disclosing that they were talking with a chatbot, makes it easier for the consumer to understand the root cause of the error,” says first author Nika Mozafari from the University of Göttingen. “A chatbot is more likely to be forgiven for making a mistake than a human.” In this scenario, customer loyalty can even improve.

Featured image: In this research study, the test subjects chatted with a chatbot – but only half of them knew that it was a non-human conversation partner. © Mozafari

Original publication: Mozafari, Nika, Weiger, Welf H. and Hammerschmidt, Maik (2021), “Trust me, I’m a bot – repercussions of chatbot disclosure in different service frontline settings”, Journal of Service Management.

Provided by University of Göttingen

Short Chain Fatty Acids: An “ACE in the Hole” Against SARS-CoV-2 Infection (Biology)

Scientists find that short chain fatty acids can be used to reduce susceptibility to SARS-CoV-2 infection and mortality from COVID-19

SARS-CoV-2, the virus responsible for the COVID-19 pandemic, is highly transmissible, with nasal passages being the target of original infection. The nasal passage also shows the highest expression of ACE2, a protein that has been widely linked with increased susceptibility to COVID-19. Now, scientists from Japan have found that nasal inflammation can influence susceptibility to SARS-CoV-2. They also identified the use of short chain fatty acids as a potential COVID-19 management strategy.

Humans are no stranger to coronavirus (CoV) pandemics. Just like SARS-CoV-2 (the virus that causes COVID-19), another member of the coronavirus family—SARS-CoV—caused the severe acute respiratory syndrome (SARS) epidemic across parts of Asia in 2003. But, its spread was contained way faster than COVID-19. So, what makes SARS-CoV-2 so contagious?

Both SARS-CoV and SARS-CoV-2 viruses bear “spike proteins” which get inside our cells by binding to a protein called angiotensin-converting enzyme 2 (ACE2) that is found in our cells. However, the SARS-CoV-2 spike (S) protein has been found to have a higher binding affinity (10 to 20 times that of SARS-CoV) to ACE2, thus establishing a link between the pathogen and the protein.

Interestingly, recent studies have shown that patients with COVID-19 who have rhinosinusitis (i.e., inflammation of the nose) have a low risk of hospitalization. Moreover, the expression of ACE2 was reduced in patients with rhinosinusitis. Coincidentally, another study has shown that short-chain fatty acids (SCFAs), produced by bacteria in the gut have beneficial effects in allergy and viral infections. These separate findings prompted an investigation of the effect that SCFAs in the nasal cavity against SARS-CoV-2 infection by scientists from the University of Fukui, Japan, led by Dr. Tetsuji Takabayashi.

In a new study published in the American Journal of Rhinology & Allergy, the scientists attempted to understand the effect of SCFAs on ACE2 expression in the nasal passage, and the potential impact on COVID-19 infection. “This is the first report that short-chain fatty acids (SCFAs) effectively reduce the ACE2 levels in human airway epithelial cells,” remarks Dr. Takabayashi.

To understand the status of ACE2 expression in patients with allergies, the researchers studied the levels of ACE2 in the inner lining of the nose in patients with seasonal allergic rhinitis induced by Japanese cedar pollen (SAR-JCP) and chronic rhinosinusitis (CRS). Using techniques like real time-PCR to quantify the expression of ACE2, the researchers found that there was no increase in ACE2 expression in in patients with SAR-JCP, whereas it was decreased in patients with CRS.

To better understand the effect of SCFAs on ACE2 expression, the researchers cultured nasal epithelial cells and exposed them to either SFCA and double-stranded RNA (similar to the nuclear material found in some viruses and known to enhance ACE2 expression). Upon examining the expression of ACE2, the researchers saw that the SFCAs had suppressed ACE2 expression in the presence of the RNA as well.

These results suggest that SFCAs has potential therapeutic applications against COVID-19. Dr. Takabayashi explains, “The nasal mucosa exhibits the highest ACE2 expression among human organs and hence is a prominent target of original infection. Therefore, the development of strategies to downregulate ACE2 expression in nasal epithelial cells could reduce SARS-CoV-2 transmission and be useful as a novel therapeutic approach.”

The team’s timely findings will certainly aid in our fight against COVID-19.

Featured image: In a recent study, scientists examined the nasal expression of ACE2 and saw that administration of SCFAs had suppressed ACE2 expression even in the presence of viral RNA. The findings suggest that SFCAs have potential therapeutic applications against COVID-19. Image courtesy: Kanako Yoshida from University of Fukui


  • Title of original paper: Regulation of the expression of SARS-CoV-2 receptor angiotensin-converting enzyme in nasal mucosa
  • Journal: American Journal of Rhinology & Allergy
  • DOI: 10.1177/19458924211027798

Provided by University of Fukui