Tag Archives: #bacteria

How A Unique Family Of Bacteria Infects The Body So Easily? (Biology)

New research from the University of Florida explains how a family of bacteria called Yersinia infects the body so successfully.

Yersinia bacteria, a family that includes the bacterium responsible for bubonic plague, is able go undetected by interrupting communication between immune system cells and the site of the infection, the researchers showed. This communication is normally mediated by specific lipids.

“We showed how Yersinia reduces the ability of an infected cell to produce a lipid called prostaglandin E2. With any bacterial infection, this lipid tells the immune system that there is a threat, but in the case of Yersinia, this communication is missing,” said Mariola Edelmann, senior author of the study and an assistant professor in the UF/IFAS department of microbiology and cell science.

“While non-steroidal anti-inflammatory drugs such as ibuprofen typically are used to block overstimulation of prostaglandin E2 production, we propose that for some infections, a moderate production of this lipid is helpful for clearance of the infection,” Edelmann added.

In effect, by blocking prostaglandin E2 synthesis, Yersinia takes away infected cells’ ability to call for help, the researchers said. Until now, scientists did not know how the bacteria were able to do this at a molecular level.

“Yersinia has a ‘secretion system,’ which is like a tiny needle the bacterium uses to introduce a set of specific enzymes into a cell, including the one that stops the cell from making prostaglandin E2,” said Austin Sheppe, first author of the study and a former graduate student in Edelmann’s lab. Sheppe earned his doctorate from the UF/IFAS College of Agricultural and Life Sciences (CALS) in 2021 and currently works as a post-doctoral associate in Dr. Aria Eshraghi’s laboratory in the UF College of Veterinary Medicine’s department of infectious diseases and immunology.

A recent review study, authored by Sheppe and Edelmann, discussing the role of prostaglandins in immune response is published in the journal Infection and Immunity.

Study: How a unique family of bacteria hides from the immune system
Mariola Edelmann in the lab. Credit: Gustavo Maegawa

Altering the production of prostaglandins to evade the immune system is unique to the Yersinia family, which includes three closely related strains: Yersinia enterocolitica and Yersinia pseudotuberculosis, which are foodborne and cause gastrointestinal illness; and Yersinia pestis, which causes bubonic plague, the same disease that killed millions in Europe during the Middle Ages.

For safety purposes and cost effectiveness, the researchers only conducted their experiment with Y. enterocolitica and Y. pseudotuberculosis. However, the molecular features that allow these Yersinia strains to interrupt communication with the immune system are also found in Y. pestis.

“Previous research shows that the human immune system has a hard time detecting and clearing Yersinia infections, but the precise mechanism was unknown,” Edelmann said. “Our findings suggest that Yersinia bacteria’s ability to dodge the immune system by avoiding the production of prostaglandin E2 may be what make them so problematic.”

Fortunately, unlike people living during the Middle Ages, people today can combat Yersinia bacteria with antibiotics. However, with antibiotic resistance on the rise, plus the fact that Y. enterocolitica causes more than 100,000 cases of foodborne illnesses a year, understanding how these bacteria operate opens doors to new treatments, Edelmann said.

“Our next step is study therapeutics that can counteract the way that Yersinia interrupts the production of prostaglandin E2. We are interested in investigating a synthetic version of the lipid, ways to inhibit the enzyme the bacteria use or make it so the lipid that is produced lasts longer,” Edelmann said.

In addition to Edelmann and Sheppe, the study’s co-authors include John Santelices, a UF/IFAS CALS doctoral student studying microbiology and cell science LS, and Daniel Czyz, assistant professor of microbiology and cell science.

The study is published in the journal Microbiology Spectrum.

Featured image: John Santelices and Mariola Edelmann in the lab. Credit: Gustavo Maegawa

Reference: Austin E. F. Sheppe et al, Yersinia pseudotuberculosis YopJ Limits Macrophage Response by Downregulating COX-2-Mediated Biosynthesis of PGE2 in a MAPK/ERK-Dependent Manner, Microbiology Spectrum (2021). DOI: 10.1128/Spectrum.00496-21

Provided by University of Florida

How Bacteria Contributes To Bacterial Vaginosis? (Medicine)

A new study examined how specific bacteria alter the vaginal microenvironment and ultimately influence the balance between health and disease.

Bacterial vaginosis is the most common and recurrent gynecological condition affecting nearly 30% of women between the ages of 15 and 44, according to the U.S. Centers for Disease Control and Prevention. A University of Arizona Health Sciences-led study recently identified a specific bacteria family and uncovered how it contributes to bacterial vaginosis, paving the way for new insights into disease prevention and treatment.

Led by Melissa Herbst-Kralovetz, PhD, a member of the BIO5 Institute and associate professor of basic medical sciences at the College of Medicine – Phoenix, researchers found that members of the Veillonellaceae bacteria family contribute to an increase in inflammation and cell death, and alter the acidity of the cervical microenvironment. These changes support bacterial vaginosis and create favorable conditions for subsequent gynecological diseases, such as sexually transmitted infections and cancer.

Melissa Herbst-Kralovetz, PhD, focuses her research on infections that impact women’s health.
Melissa Herbst-Kralovetz, PhD, focuses her research on infections that impact women’s health. © University of Arizona

“Bacterial vaginosis is an enigma,” said Dr. Herbst-Kralovetz, who is also director of the Women’s Health Research Program. “We know many factors contribute to this disease, but little is known about the functional impact of the major players and how they’re changing the local landscape.”

The paper, “Veillonellaceae family members uniquely alter the cervical metabolic microenvironment in a human three-dimensional epithelial model,” published July 6 in the journal npj Biofilms and Microbiomes, found that Veillonellaceae family members contribute to disease by altering inflammation and metabolism in the cervicovaginal region.

The female reproductive tract is typically colonized by bacteria that promote health, such as Lactobacillus. While these bacteria are considered friendly, an imbalance can lead to the creation of a biofilm – a consortium of many different harmful microbes – that promotes disease.

Last year, Dr. Herbst-Kralovetz and colleagues described a hypothetical model in which the interactions between microbes and human cells alter the vaginal microenvironment and ultimately influence the balance between health and disease. This study is the first to define a definitive role for this bacterial family in bacterial vaginosis.

Using a 3D human model, Dr. Herbst-Kralovetz’s group evaluated the effects of three bacterium – Veillonella atypicaVeillonella montpellierensis, and Megasphaera micronuciformis – on the cervical microenvironment.

They found that two species – V. atypica and V. montpellierensis – decreased lactate, an acid typically produced by beneficial bacteria that provides protection from harmful infections. These two species also increased substances that play a role in bacterial vaginosis-associated vaginal odor.

They also found that M. micronuciformis further drives disease progression by increasing inflammation and promoting cell death through the production of certain fat molecules.

Insights from this study lay the foundation for polymicrobial, or “multi-bug” studies, which can determine the complex interaction effects of multiple bacterial species on female reproductive health.

“Using this study and our 3D model as a foundation, we hope to determine if and how other species are altering the environment to contribute to bacterial vaginosis,” Dr. Herbst-Kralovetz said. “We have found that different species have distinct contributions, so we also hope to categorize a variety of bacterial vaginosis -associated microbes based on their unique effects on the female reproductive tract.”

Ultimately, Dr. Herbst-Kralovetz says this study and others like it can help to inform treatment and intervention strategies.

“It is important to know who the major players are, but also how they’re influencing physiological processes and disease, so we can develop targeted strategies to treat bacterial vaginosis and prevent subsequent gynecological infections and cancer,” she said.

Dr. Herbst-Kralovatz’s co-authors from the College of Medicine – Phoenix are Jason Maarsingh, PhD, a postdoctoral research assistant in the Department of Obstetrics and Gynecology, and Pawel Laniewski, PhD, an assistant research scientist in the Department of Basic Medical Sciences. Other co-authors include undergraduate student Camryn Garza and Mary Salliss, who participated in the Bath University Placement/Exchange Program.

The study was funded in part by the National Cancer Institute, a division of the National Institutes of Health, and a supplement from the Office of Research for Women’s Health (3P30CA023074-39S3), and the Flinn Foundation (2244).

Provided by University of Arizona Health Sciences

A Mechanism Through Which ‘Good’ Viruses Kill ‘Bad’ Bacteria And Block Their Reproduction (Biology)

An important step in the battle against antibiotic-resistant bacteria

The battle against antibiotic-resistant bacteria: A new study at Tel Aviv University revealed a mechanism through which “good” viruses can attack the systems of “bad” bacteria, destroy them and block their reproduction. The researchers demonstrated that the “good” virus (bacteriophage) is able to block the replication mechanism of the bacteria’s DNA without damaging its own, and note that the ability to distinguish between oneself and others is crucial in nature. They explain that their discovery reveals one more fascinating aspect of the mutual relations between bacteria and bacteriophages and may lead to a better understanding of bacterial mechanisms for evading bacteriophages, as well as ways for using bacteriophages to combat bacteria.

The study, published recently in PNAS – Proceedings of the National Academy of Sciences, was led by Prof. Udi Qimron, Dr. Dor Salomon, Dr. Tridib Mahata and Shahar Molshanski-Mor of the Sackler Faculty of Medicine. Other participants included Prof. Tal Pupko, Head of the Shmunis School of Biomedicine and Cancer Research and also of the new AI and Data Science Center ; Dr. Oren Avram of the George S. Wise Faculty of Life Sciences; and Dr. Ido Yosef, Dr. Moran Goren, Dr. Miriam Kohen-Manor and Dr. Biswanath Jana of the Sackler Faculty of Medicine.

The bacteriophage protein (green) does not kill bacteria when the DNA repair protein is absent (left). It kills bacteria by inhibiting division (elongated bacteria) only when the DNA repair protein is present (right). © Dr. Tridib Mahata.

Prof. Qimron explains that the antibiotic resistance of bacteria is one of the greatest challenges faced by scientists today. One potential solution may lie in further investigation of the targeted eradication of bacteria by “good” bacteriophages; namely, understanding bacteriophage mechanisms for taking over bacteria as a basis for the development of new tools to combat bacterial pathogens.

With this intention in mind, the current study unveiled the mechanism by which the bacteriophage takes control of the bacteria. The researchers found that a bacteriophage protein uses a DNA-repair protein in the bacteria to “cunningly” cut the bacteria’s DNA as it is being repaired. Since the bacteriophage’s own DNA has no need for this specific repair protein, it is protected from this nicking procedure. In this way the “good” bacteriophage does three important things: it distinguishes between its own DNA and that of the bacteria, destroys the bacteria’s genetic material, and blocks the bacteria’s propagation and cell division.

Prof. Qimron adds: “The bacteriophage takes advantage of the bacterial DNA’s need for repair, while the bacteriophage itself has no need for this specific kind of repair. In this way the bacteriophage destroys the bacteria without suffering any damage to itself. The ability to distinguish between oneself and others is of enormous importance in nature and in various biological applications. Thus, for example, all antibiotic mechanisms identify and neutralize bacteria only, with minimal effect on human cells. Another example is our immune system, which is geared toward maximum damage to foreign factors, with minimal self-injury.”

The researchers discovered the process by searching for types of bacterial variants not impacted by this bacteriophage mechanism – those that have developed “immunity” to it. This inquiry led them to the specific bacterial mechanisms affected by the bacteriophage takeover. “We found that the ‘immune’ bacterial variants simply stopped repairing their DNA in ways that are vulnerable to the bacteriophage attack, thereby evading the bacteriophage’s destructive mechanism. Shedding more light on the ways in which bacteriophages attack bacteria, our findings may serve as a tool in the endless battle against antibiotic-resistant bacteria,” concludes Prof. Qimron.

Featured image: Elongation of bacteria due to inhibition of division is caused by the bacteriophage protein © Dr. Tridib Mahata.

Reference: Tridib Mahata, Shahar Molshanski-Mor, Moran G. Goren, Biswanath Jana, Miriam Kohen-Manor, Ido Yosef, Oren Avram, Tal Pupko, Dor Salomon, Udi Qimron, “A phage mechanism for selective nicking of dUMP-containing DNA”, PNAS June 8, 2021 118 (23) e2026354118; https://doi.org/10.1073/pnas.2026354118

Provided by Tel-Aviv University

Adding Antibodies to Enhance Photodynamic Therapy For Viral and Bacterial Disease (Medicine)

Advancing PDT as a rapid response to pandemics

The COVID-19 pandemic has reinforced the pressing need to mitigate a fast-developing virus as well as antibiotic-resistant bacteria that are growing at alarming rates worldwide.

Photodynamic therapy (PDT), or using light to inactivate viruses, bacteria, and other microbes, has garnered promising results in recent decades for treating respiratory tract infections, such as pneumonia, and some types of cancer.

In Applied Physics Reviews, by AIP Publishing, researchers at Texas A&M University and the University of São Paulo in Brazil review the existing approaches and propose adding antibodies to enhance PDT efficacy. They provide a model to help expedite overall PDT development as a rapid response to emergent viral pandemic threats. The research is based on physical principles to target a wide range of diseases.

“The COVID-19 pandemic calls for extraordinary measures to address current gaps in the therapeutic treatment of infectious diseases, in general, and viral agents, in particular,” author Vladislav Yakovlev said. “We show how photodynamic therapy can be capable of providing an inexpensive alternative strategy in the fight against viral and bacterial infections.”

In PDT, photosensitizers (dyes and other light-reacting compounds) are typically administered intravenously or applied on the skin where treatment is needed. Microbes or cancer cells absorb the photosensitizers. The compounds react to light from a laser to form reactive oxygen species, toxic oxygen molecules that kill the cancer cells or pathogen.

One of the most promising PDT methods highlighted by the researchers is antibody PDT, or aPDT. The method involves attaching photosensitizers to viral antibodies to increase the immune response. The antibody is modified by attaching a small light-absorbing molecule, which upon illumination, can transfer the photon energy to the targeted virus particles, resulting in their destruction while reducing harm to host cells and healthy tissue.

“The aPDT process is characterized by high selectivity, rapid microbial killing, minimal invasiveness, and low occurrence of side effects,” Yakovlev said. “It also ideal for repetitive application without the concern of bacterial resistance.”

The researchers developed a mathematical model to compare PDT to other antiviral treatment by focusing on three parameters critical in modifying the treatment response to determine efficacy: photosensitizer, light, and oxygen.

Molecular oxygen is considered intrinsic to the biological system since it is present at the site of infection. On the other hand, the light dose and the photosensitizer concentration are flexible parameters to achieve efficient results in treatment.

Research protocols, therefore, should consider not only the photosensitizing molecule appropriate to the biological target and adequate wavelength but also the photosensitizer concentration, incubation time, and light dose.

The article “Photodynamic viral inactivation: Recent advances and potential applications” is authored by Jace A. Willis, Vsevolod Cheburkanov, Giulia Kassab, Jennifer M. Soares, Kate C. Blanco, Vanderlei X. Bagnato, and Vladislav V. Yakovlev. The article will appear in Applied Physics Reviews on May 18, 2021 (DOI: 10.1063/5.0044713). After that date, it can be accessed at https://aip.scitation.org/doi/10.1063/5.0044713.

Featured image: Schematic illustration of photodynamic inactivation of various viruses. © Vladislav Yakovlev/Texas A&M University

Provided by American Institute of Physics

Rooting the Bacterial Tree Of Life (Biology)

Scientists now better understand early bacterial evolution, thanks to new research featuring University of Queensland researchers.

Bacteria comprise a very diverse domain of single-celled organisms that are thought to have evolved from a common ancestor that lived more than three billion years ago.

Professor Phil Hugenholtz, from the Australian Centre for Ecogenomics in UQ’s School of Chemistry and Molecular Biosciences, said the root of the bacterial tree, which would reveal the nature of the last common ancestor, is not agreed upon.

“There’s great debate about the root of this bacterial tree of life and indeed whether bacterial evolution should even be described as a tree has been contested,” Professor Hugenholtz said.

“This is in large part because genes are not just shared ‘vertically’ from parents to offspring, but also ‘horizontally’ between distant family members.

“We’ve all inherited certain traits from our parents, but imagine going to a family BBQ and suddenly inheriting your third cousin’s red hair.

“As baffling as it sounds, that’s exactly what happens in the bacterial world, as bacteria can frequently transfer and reconfigure genes horizontally across populations quite easily.

“This might be useful for bacteria but makes it challenging to reconstruct bacterial evolution.”

For the bacterial world, many researchers have suggested throwing the ‘tree of life’ concept out the window and replacing it with a network that reflects horizontal movement of genes.

“However, by integrating vertical and horizontal gene transmission, we found that bacterial genes travel vertically most of the time – on average two-thirds of the time – suggesting that a tree is still an apt representation of bacterial evolution,” Professor Hugenholtz said.

“The analysis also revealed that the root of the tree lies between two supergroups of bacteria, those with one cell membrane and those with two.

“Their common ancestor was already complex, predicted to have two membranes, the ability to swim, sense its environment, and defend itself against viruses.”

The University of Bristol’s Dr Tom Williams said this fact led to another big question.

“Given the common ancestor of all living bacteria already had two membranes, we now need to understand how did single-membrane cells evolve from double-membraned cells, and whether this occurred once or on multiple occasions,” Dr Williams said.

“We believe that our approach to integrating vertical and horizontal gene transmission will answer these and many other open questions in evolutionary biology.”

The research was a collaboration between UQ, the University of Bristol in the UK, Eötvös Loránd University in Hungary, and NIOZ in the Netherlands, and has been published in Science (DOI: 10.1126/science.abe5011).

Featured image: Fusobacteria, Gracilicutes and Bacteroidota all branched off from a last bacterial common ancestor. © University of Queensland

Provided by University of Queensland Australia

Bacteria and Viruses Infect Our Cells Through Sugars: Now Researchers Want to Know How They Do It (Medicine)

Most infectious bacteria and viruses bind to sugars on the surface of our cells. Now researchers from the University of Copenhagen have created a library of tens of thousands of natural cells containing all the sugars found on the surface of our cells. The library may help us understand the role played by sugars and their receptors in the immune system and the brain, the researchers behind the study explain.

Sugar is not just something we eat. On the contrary. Sugar is one of the most naturally occurring molecules, and all cells in the body are covered by a thick layer of sugar that protects the cells from bacteria and virus attacks. In fact, close to 80 per cent of all viruses and bacteria bind to the sugars on the outside of our cells.

Sugar is such an important element that scientists refer to it as the third building block of life – after DNA and protein. And last autumn, a group of researchers found that the spike protein in corona virus needs a particular sugar to bind to our cells efficiently.

Now the same group of researchers have completed a new study that further digs into the cell receptors to which sugars and thus bacteria and virus bind.

‘We have established how the sugars bind to and activate the so-called Siglec receptors that regulate immunity. These receptors play a major role, as they tell the immune system to decrease or increase activities. This is an important mechanism in connection with autoimmune diseases’, says the first author of the study, Postdoc Christian Büll from the Copenhagen Center for Glycomics (CCG) at the University of Copenhagen.

Lead author Christian Büll working with the new technology (photo: Mel Robbins).

The unique sugar language

When the immune system receives wrong signals, it can lead to autoimmune diseases, which is when the immune system attacks itself. The Siglec receptors receive signals via the sialic acid sugar, a carbohydrate that typically closes the sugar chains on the surface of our cells. When Siglec receptors meet the right sugar chains, the immune system is told to dampen or activate.

‘As part of the new study, we have created a cell library that can be used to study how various sugars bind to and interact with receptors. We have done this by creating tens of thousands of cells each containing a bit of the  unique sugar language, which enables us to distinguish them from one another and to study their individual effect and process. This knowledge can help us develop better treatment options in the future’, says Associate Professor Yoshiki Narimatsu from CCG, who also contributed to the study.

‘The surface of the cells in the library is the same as the one found on cells in their natural environment. This means that we can study the sugars in an environment with the natural occurrence of e.g. proteins and other sugars, and we can thus study the cells in the form in which virus and bacteria find them’, Yoshiki Narimatsu explains.

Important discovery for Alzheimer’s

Working on the new study, the researchers identified the sugars that bind to the specific receptor that plays a main role in the development of Alzheimer’s disease.

‘Our main finding concerns the Siglec-3 receptor. Mutations in the Siglec-3 receptor is already known to play a role in connection with Alzheimer’s, but we did not know what the receptor specifically binds to. Our method has now identified a potential natural sugar that binds specifically to the Siglec-3 receptor. This knowledge represents an important step forwards in understanding the genetic defects that cause a person to develop the disease’, says Christian Büll.

The creation of the sugar libraries was funded by the Lundbeck Foundation and the Danish National Research Foundation.

Read the entire study, ‘Display of the Human Mucinome with Defined O-Glycans by Gene Engineered Cells’, here.

Featured Photo: Many bacteria and viruses depend on sugars to infect our cells. And last autumn, the same team of researchers discovered found that the spike protein in corona virus needs a particular sugar to bind to our cells efficiently.

Provided by University of Copenhagen

Superbug Killer: New Nanotech Destroys Bacteria And Fungal Cells (Material Science)

Nanothin antimicrobial coating could prevent and treat potentially deadly infections

Researchers have developed a new superbug-destroying coating that could be used on wound dressings and implants to prevent and treat potentially deadly bacterial and fungal infections.

The material is one of the thinnest antimicrobial coatings developed to date and is effective against a broad range of drug-resistant bacteria and fungal cells, while leaving human cells unharmed.

Antibiotic resistance is a major global health threat, causing at least 700,000 deaths a year. Without the development of new antibacterial therapies, the death toll could rise to 10 million people a year by 2050, equating to $US100 trillion in health care costs.

While the health burden of fungal infections is less recognised, globally they kill about 1.5 million people each year and the death toll is growing. An emerging threat to hospitalised COVID-19 patients for example is the common fungus, Aspergillus, which can cause deadly secondary infections.

The new coating from a team led by RMIT University in Melbourne, Australia, is based on an ultra-thin 2D material that until now has mainly been of interest for next-generation electronics.

Studies on black phosphorus (BP) have indicated it has some antibacterial and antifungal properties, but the material has never been methodically examined for potential clinical use.

The new research, published in the American Chemical Society’s journal Applied Materials & Interfaces, reveals that BP is effective at killing microbes when spread in nanothin layers on surfaces like titanium and cotton, used to make implants and wound dressings.

Co-lead researcher Dr Aaron Elbourne said finding one material that could prevent both bacterial and fungal infections was a significant advance.

“These pathogens are responsible for massive health burdens and as drug-resistance continues to grow, our ability to treat these infections becomes increasingly difficult,” Elbourne, a Postdoctoral Fellow in the School of Science at RMIT, said.

“We need smart new weapons for the war on superbugs, which don’t contribute to the problem of antimicrobial resistance.

“Our nanothin coating is a dual bug killer that works by tearing bacteria and fungal cells apart, something microbes will struggle to adapt to. It would take millions of years to naturally evolve new defences to such a lethal physical attack.

“While we need further research to be able to apply this technology in clinical settings, it’s an exciting new direction in the search for more effective ways to tackle this serious health challenge.”

Co-lead researcher Associate Professor Sumeet Walia, from RMIT’s School of Engineering, has previously led groundbreaking studies using BP for artificial intelligence technology and brain-mimicking electronics.

“BP breaks down in the presence of oxygen, which is normally a huge problem for electronics and something we had to overcome with painstaking precision engineering to develop our technologies,” Walia said.

Candida auris fungus before exposure to ultrathin layers of black phosphorous (left) and after (right). © RMIT University

“But it turns out materials that degrade easily with oxygen can be ideal for killing microbes – it’s exactly what the scientists working on antimicrobial technologies were looking for.

“So our problem was their solution.”

How the nanothin bug killer works

As BP breaks down, it oxidises the surface of bacteria and fungal cells. This process, known as cellular oxidisation, ultimately works to rip them apart.

In the new study, first author and PhD researcher Zo Shaw tested the effectiveness of nanothin layers of BP against five common bacteria strains, including E. coli and drug-resistant MRSA, as well as five types of fungus, including Candida auris.

In just two hours, up to 99% of bacterial and fungal cells were destroyed.

Importantly, the BP also began to self-degrade in that time and was entirely disintegrated within 24 hours – an important feature that shows the material would not accumulate in the body.

The laboratory study identified the optimum levels of BP that have a deadly antimicrobial effect while leaving human cells healthy and whole.

The researchers have now begun experimenting with different formulations to test the efficacy on a range of medically-relevant surfaces.

The team is keen to collaborate with potential industry partners to further develop the technology, for which a provisional patent application has been filed.

The RMIT research team also included: Sruthi Kuriakose and Dr Taimur Ahmed (Engineering); Samuel Cheeseman, Dr James Chapman, Dr Nhiem Tran, Professor Russell Crawford, Dr Vi Khanh Truong, Patrick Taylor, Dr Andrew Christofferson, Professor Michelle Spencer and Dr Kylie Boyce (Science); and Dr Edwin Mayes (RMIT Microscopy and Microanalysis Facility).

Broad-spectrum solvent-free layered black phosphorus as a rapid action antimicrobial‘, with collaborators from Swinburne University of Technology and Deakin University, is published in ACS Applied Materials & Interfaces (DOI: 10.1021/acsami.1c01739).

Featured image: A fungal cell (green) interacting with a nanothin layer of black phosphorous (red). Image magnified 25,000 times. © RMIT University

Provided by RMIT University

Gut Bacteria “Talk” To Horse’s Cells to Improve Their Athletic Performance (Biology)

Study linking gut bacteria to more efficient energy generation in the cells of horses paves the way for dietary supplements that enhance their performance

A horse’s gut microbiome communicates with its host by sending chemical signals to its cells, which has the effect of helping the horse to extend its energy output, finds a new study published in Frontiers in Molecular Biosciences. This exciting discovery paves the way for dietary supplements that could enhance equine athletic performance.

“We are one of the first to demonstrate that certain types of equine gut bacteria produce chemical signals that communicate with the mitochondria in the horse’s cells that regulate and generate energy,” says Eric Barrey, author of this study and the Integrative Biology and Equine Genetics team leader at the National Research Institute for Agriculture, Food and Environment, France. “We believe that metabolites – small molecules created by breaking down bigger molecules for food or growth – produced by these bacteria have the effect of delaying low blood sugar and inflammation in the cells, which in turn extends the horse’s athletic performance.”

Links to disease

Mitochondria, which can be briefly described as the energy provider of cells, have been shown in recent studies to be interdependent with gut bacteria. In fact, many diseases associated with mitochondrial dysfunction in humans, such as Parkinson’s and Crohn’s have been linked to changes in the gut microbiome in many previous studies.

“Studying horses is a good way to assess the link between gut bacteria and mitochondria, because the level of exercise, and thereby mitochondrial function, performed by a horse during an endurance race is similar to that of a human marathon runner,” explains Dr Nuria Mach, first author of this paper, also based at the National Research Institute for Agriculture, Food and Environment, France.

She continues, “For this study we gained permission for veterinary doctors to take blood samples from 20 healthy horses of similar age and performance level, at the start and end of the International Endurance Competition of Fontainebleau, an 8-hour horse race in France. These samples provided information about the chemical signals and expression of specific genes, which is the process by which DNA is converted into instructions for making proteins or other molecules. To understand the composition of the horse’s gut bacteria metabolites, we obtained fecal samples at the start of the race.”

The researchers found that certain bacteria in the gut were linked to the expression of genes by the mitochondria in the cells. Furthermore, the genes that were expressed, or “turned on”, were linked to activities in the cell that helped it to adapt to energetic metabolism.

Evolutionary explanation

“Interestingly, mitochondria have a bacterial origin – it is thought they formed a symbiotic relationship with other components to form the first cell. This may explain why mitochondria have this line of communication with gut bacteria,” says Barrey.

Mach concludes, “Improving our understanding of the intercommunication between the horse and the gut microbiome could help enhance their individual performance, as well as the method by which they are trained and dietary composition intake. Manipulating the gut microbiota with probiotic supplements as well as prebiotics, to feed the good bacteria, could be a way for increasing the health and balance of the microbiome and horses, to better sustain endurance exercise.”

Featured image: A typical endurance horse (Arabian breed) presented for a gait test before the start of the race to check locomotor soundness. During an endurance competition (100-160 km), horses must undergo veterinary inspection at the end of each 20 to 40 km loop to check their recovery and capacity to continue the race under good health conditions. The energetic expenditure during an endurance race is very high, so an interesting model to show the functional relationship between the microbiota profile and energetic metabolism at the level of the mitochondria. © Eric Barrey

Reference: Núria Mach, Marco Moroldo, Andrea Rau, Jérôme Lecardonnel, Laurence Le Moyec, Céline Robert and Eric Barrey, “Understanding the holobiont: crosstalk between gut microbiota and mitochondria during long exercise in horse”, Front. Mol. Biosci. | doi: 10.3389/fmolb.2021.656204

Provided by Frontiers

Use Virus Fight Against Bacteria? New Antibacterial Materials Found base on Viruses (Chemistry)

Chinese scientists have recently exploited a new strategy to enhance peptides’ activity against Gram-negative bacteria effectively by conjugating the peptides onto a rod-like virus.  

The work, published online in Nano Letters, was conducted by Prof. NIU Zhongwei and Associate Prof. TIAN Ye from the Technical Institute of Physics and Chemistry (TIPC) of the Chinese Academy of Sciences (CAS).  

Gram-negative bacteria and infection problems caused are threatening global health. Antibiotic resistance is also a serious worldwide problem. Therefore, antimicrobial peptides, which lead to little antibiotic resistance, are regarded as the most promising alternatives to antibiotics. However, compared with the antibiotics, the efficiencies and minimum inhibitory concentration of existing peptides are lower. The clinical applications of peptides are limited.  

In this work, the peptides were “decorated” by conjugating onto one-dimensional rod-like tobacco mosaic virus (TMV). The conjugated peptides could achieve an obvious increased local concentration on the TMV surface. Meanwhile, the interaction area between a rod-like nanoparticle and bacterial cell membrane is becoming larger than the normal area between a spherical nanoparticle and bacterial cell membrane. With the interaction area increased, the destruction to the bacterial cell membrane is stronger.  

As a result, the antibacterial ability of the peptides on the generated peptide-conjugated TMV nanoparticles (peptide-TMV) has extremely enhanced and even achieved hundred times level than free peptides.    

Besides, the conjugated peptides have obtained the ability to inhibit biofilm formation. Through morphology and gene detection of Escherichia coli (E. coli), the damage to E. coli was caused by the destruction of membrane structure, which led to a high osmotic pressure and the generation of reactive oxygen species.  

By experiencing the process, E. coli cell died as the gene expression of biofilm growth was inhibited, and finally biofilm inhibition was achieved. 

This work was supported by the National Key R&D Program, the National Natural Science Foundation of China, the Beijing Natural Science Foundation and the Presidential Foundation of TIPC.  

Featured image: Schematic Illustration of the Peptide-TMV inducing Bacteria‘s Death and Inhibiting Biofilm Formation. (Image by NIU et al.) 


Conjugating Peptides onto 1D Rodlike Bionanoparticles for Enhanced Activity against Gram-Negative Bacteria

Provided by Chinese Academy of Sciences