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Research led by Washington State University scientists supports a novel theory that the innate immune system people are born with can respond differently to specific pathogens. This quality, known as immunological specificity, was previously ascribed only to the adaptive immune system, which develops over time through disease exposure.
Published in the journal Cell Reports, the study suggests that this innate immune specificity is driven by the nervous system and identifies a neuronal protein as a critical link in the process.
Based on an animal model, these findings hold early promise for the treatment of conditions such as sepsis, arthritis and inflammatory bowel disease, in which the innate immune system attacks the body and causes uncontrolled inflammation. They could also provide the basis for finetuning an experimental treatment that harnesses the nervous system to fight infection.
“Clinical studies have shown that stimulating impaired neural circuits — either electrically or pharmacologically — can cure or alleviate many innate immune diseases,” said Jingru Sun, co-senior author on the study and an associate professor in the WSU Elson S. Floyd College of Medicine. “Knowing how the innate immune system generates a specific response to a particular pathogen enables us to manipulate neural circuits to adjust the intensity of the immune response as needed.”
This would essentially help restore balance to the immune system, either by dialing back an excessive response that can cause prolonged inflammation, tissue damage and even death; or by boosting an insufficient response to keep an infection from getting worse. Sun said the latter is particularly significant given that the “post-antibiotic era” is fast approaching — a time when existing antibiotics will be useless in the fight against drug-resistant superbugs.
The research was conducted in a tiny worm known as Caenorhabditis elegans(C. elegans) that feeds on bacteria in soil. C. elegans is a commonly used model animal for studying the neural regulation of innate immunity because of its simple nervous system with only 302 well-identified neurons — versus 86 billion neurons in a human brain — and its transparent body that allows scientists to see how different genes are expressed. What’s more, unlike humans, C. elegans lacks an adaptive immune system, making it possible to study the specificity of its innate immune system without interference from adaptive immune responses.
Initial studies by the WSU team had found that the absence of a neuronal receptor protein known as NMUR-1 had varying effects on the survival of C. elegans when exposed to different bacterial pathogens, indicating that NMUR-1 might mediate the specificity of the innate immune response to infection. Further testing with two bacteria that showed opposite effects on survival — i.e., longer and shorter lifespan — confirmed that NMUR-1 drives innate immune specificity and also revealed how the protein drives different responses to different pathogens.
“What we found is that NMUR-1 controls transcription factors, which in turn control the transcription of distinct innate immune genes in response to different pathogens,” said co-senior author Yiyong Liu, an assistant professor in the WSU Elson S. Floyd College of Medicine and director of the university’s Genomics Service Center.
First author Phillip Wibisono, a WSU graduate student, said the next steps in this research are to identify which neural circuits NMUR-1 are a part of and then treat those neural circuits to see how that alters the immune response to different pathogens. If successful, that would bring their work closer to potential applications in human treatment.
In addition to Sun, Liu, and Wibisono, co-authors on the paper include Shawndra Wibisono, Chia-Hui Chen and Durai Sellegounder of the WSU Elson S. Floyd College of Medicine, and Jan Watteyne and Isabel Beets at KU Leuven in Belgium.
The study was supported by the National Institute of General Medical Sciences, a component of the National Institutes of Health, with additional funds provided by Research Foundation Flanders and the WSU Elson S. Floyd College of Medicine.
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Materials provided by Washington State University. Original written by Judith Van Dongen. Note: Content may be edited for style and length.

By systematically analyzing epigenetic changes in angiogenesis-stimulated vascular endothelial cells, Professor Takashi Minami (Kumamoto University, Japan) and his team have found a unique epigenetic modification (bivalent histone-mark switch) specific to critical transcription factors that induce genes essential for angiogenesis and revealed that the histone modifiers responsible for this modification are vital for postnatal angiogenesis.
Although comprehensive epigenetic datasets, especially in cancer cells or stem (ES/iPS) cells, have been constructed, the changes in epigenome dynamics in normal vascular endothelial cells upon angiogenesis stimulation are still not completely understood. New research from Dr. Minami is expected to lead to the compilation of an epigenomic database for normal endothelial cells and selective epigenomic drug discovery to protect against age-related vascular diseases.
The vascular network that extends throughout the body is the foundation of the biological homeostasis that keeps the body in a steady state. Endothelial cells form the basis of these blood vessels, and their proper functioning is necessary for human health. If the vascular system is over-activated or activated at misplaced regions, it may lead to cancer, heart disease, or cerebrovascular disease. However, revealing the detailed mechanisms of endothelial cell activation-mediated postnatal angiogenesis and epigenomic changes has proven to be challenging research.
To tackle this problem, Dr. Minami and his team conducted a genome-wide analysis of epigenetic changes (mRNAs and histone modification changes) in VEGF (vascular endothelial growth factor essential for angiogenesis) signaling over a minute-by-minute basis. They then cataloged and mapped the changes to understand where changes occurred. In addition, they used a mouse model to evaluate whether the histone-mark changes from their comprehensive database are critical for postnatal angiogenesis.
They found that when vascular endothelial cells receive VEGF signaling, a unique “bivalent histone switch” that is limited to immediate-early type transcription factors essential for angiogenesis is triggered, coinciding with the timing of the transfer of the transcription factor NFAT (which is involved in, among other things, the immune response and cardiac muscle development) into the nucleus.
The term “bivalent” refers to the fact that H3K27me3 (a transcriptional brake) and H3K4me3 (a transcriptional accelerator), which mark epigenetic histone modifications, coexist in the region where transcription factors are expressed. The two marks (H3K27me3 and H3K4me3) are known to occur in the regulatory region of transcription factor expression during the differentiation of stem (ES/iPS) cells. However, the bivalent switch in endothelial cells is highly dynamic and specific, occurring in the gene region of a group of angiogenesis-inducing/-essential transcription factors fully enriched in H3K27me3 brake marks. The non-canonical PRC1 is considered to be functionally different from the canonical PRC1. In the endothelium, non-canonical PRC1.3 binds to this genomic region 15 minutes after VEGF stimulation and disables brakes until the canonical PRC1-brake returns to the endothelium at 60 minutes. After 15 minutes of VEGF treatment, and at the same time as NFAT nuclear localization, NFAT interacts with PTIP-triggered H3K4me3 markers at the region of immediate-early type transcription factors, resulting in an angiogenesis-specific bivalent switch. PTIP is a component (guidance factor) of the MLL3/4, H3K4me3 marking enzyme.
The researchers also found endothelial cell-specific removal of PRC1.3 and PTIP suppressed only postnatal VEGF-induced angiogenesis without affecting developmental blood vessels, thereby delaying cancer growth and suppressing pathological inflammation.
Recently, the epigenome has come to be regarded as “chromatin biology” and includes histone modifications and nuclear structures. It has been mainly studied in ES/iPS cells and cancer cells. This is the first time an epigenetic database of normal endothelial cells has been established. The researchers expect that it will lay the foundation for endothelial activation analyses, which will lead to the future of angiogenesis research.
Dr. Minami commented that, “We believe that the development of drugs that specifically inhibit PTIP-NFAT interaction, as well as epigenomic drugs focused on non-canonical PRC1.3, are expected to lead the way to selective drug discovery that will protect against the vascular diseases found in aging.”
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Materials provided by Kumamoto University. Note: Content may be edited for style and length.

Researchers at the University of Toronto and University Health Network have shown how probiotic bacteria in the gut could undermine immunity in pancreatic cancer, pointing toward more personalized cancer treatments.
Lactobacillus — a type of bacteria thought to promote gut health — can alter the function of immune cells called macrophages in the pancreatic tumour environment and spur cancer growth, the researchers found.
“Most studies focus on positive correlations between the microbiome and cancer outcomes,” said Tracy McGaha, a professor of immunology at U of T’s Temerty Faculty of Medicine and a senior scientist at Princess Margaret Cancer Centre, University Health Network. “This work focused on negative correlations of the microbiome with cancer, and suggests that in some conditions, the constituency of the microbiome may have a negative impact.”
The journal Immunity published the results today.
Macrophages are tissue-resident immune cells thought to play an important role in tumour growth and metastasis. The researchers showed that Lactobacillus affects macrophage function by metabolizing dietary tryptophan, an essential amino acid found in protein from plant- and animal-based foods.
Indoles, a class of metabolites resulting from microbial tryptophan metabolization, activate the aryl hydrocarbon receptor, or AHR — a protein that regulates gene expression, and which can enable both beneficial inflammation and immune suppression in other areas of the body.

Researchers have identified a powerful combination of antivirals to treat COVID-19. Combining the drug brequniar with remdesivir or molnupiravir — both approved by the U.S. Food and Drug Administration for emergency use — inhibited the SARS-CoV-2 virus in human respiratory cells and in mice, according to a new study led by researchers in the Perelman School of Medicine at the University of Pennsylvania and the University of Maryland School of Medicine. The findings, published this week in Nature, suggest that these drugs are more potent when used in combination than individually.
Though they have not yet been tested in clinical trials, the combinations of drugs identified in their study have the potential to become very promising COVID-19 treatments, says principal investigator Sara Cherry, PhD, a professor of Pathology and Laboratory Medicine at Penn, who led the research with David Schultz, PhD, technical director of the Penn High-Throughput Screening Core, and Matthew Frieman, PhD, of the Center for Pathogen Research at the University of Maryland School of Medicine, along with collaborators from the National Institutes of Health.
“Identifying combinations of antivirals is really important, not only because doing so may increase the drugs’ potency against the coronavirus, but combining drugs also reduces the risk of resistance,” Cherry said.
SARS-CoV-2, the virus that causes COVID-19, has infected 382 million people and led to 5 million deaths worldwide. There remains an urgent need for therapeutics to treat COVID-19, which has been amplified by the emerging threats of new variants that may evade vaccines. In response to this demand, Cherry and a team of collaborators have screened 18,000 drugs in search of antiviral activity, using live SARS-CoV-2 infection in human respiratory epithelial cells, because lung cells are the major target for the virus.
The researchers identified 122 drugs that showed antiviral activity and selectivity against the coronavirus, including 16 nucleoside analogs — the largest category of antivirals that are used clinically. Among the 16 were remdesivir, which is given by injection into a vein and has been approved by the FDA to treat COVID-19, and molnupiravir, an oral pill that was authorized for use in December.
Also among the 122 drug candidates, the researchers identified a panel of host nucleoside biosynthesis inhibitors, including the experimental drug brequinar. Nucleoside biosynthesis inhibitors work by blocking the body’s own enzymes from making nucleosides, which prevents the virus from being able to “steal” RNA building blocks and replicate. Brequinar is currently being tested in clinical trials as a COVID-19 treatment and as part of a potential combination therapy for some cancers.

Researchers at the University of British Columbia are shedding new light on the molecular factors that give COVID-19 variants a competitive edge — essential knowledge that could improve disease management as new variants continue to emerge.
The study, published in Nature Communications, examines the structural and biochemical properties of the Kappa and Delta variants, which co-emerged in India in late 2020. The findings explain how the Delta variant may have been able to beat out the Kappa variant and become dominant across the globe.
“We are at a point in the pandemic where new variants continue to emerge and compete with each other. It’s very much survival of the fittest,” said senior author Dr. Sriram Subramaniam, professor in UBC’s faculty of medicine. “Understanding the factors that underpin the ‘fitness’ of each variant will allow us to respond more effectively to emerging threats and better target treatments.”
For the study, the researchers used cryo-electron microscopy (cryo-EM) to examine the atomic-level structure of the Delta and Kappa viral spike proteins, as well as biochemical studies to assess how strongly the spike protein binds with the ACE2 receptor on human cells.
“The spike protein extends from the surface of the virus and binds with the ACE2 receptor in order to infect human cells, like a key being inserted into a lock,” explains Dr. Subramaniam.
The researchers found that both variants display evasion from antibodies that target a specific part of the spike protein, known as the N-terminal domain. However, when compared to the Kappa variant and wild-type COVID-19, the Delta variant spike protein was shown to create stronger bonds with the human ACE2 receptor.
“The combination of increased antibody escape and enhanced ACE2 binding provides an explanation, in part, for the rapid global dominance of the Delta variant,” said Dr. Subramaniam.
Notably, the Kappa variant spike protein displayed an unusual property, where two Kappa spike proteins were able to join together in what’s known as a “stacked head-to-head dimer” — a structure not yet seen in any other COVID-19 variant. The researchers say it is not clear if this unexpected feature was one of the molecular factors that led to Kappa being outcompeted by the Delta variant.
“There is much that we still don’t understand about the subtle molecular features that determine the overall fitness of these variants,” said Dr. Subramaniam.
In a previous study published in Science, Dr. Subramaniam and his team used cryo-EM to perform a structural analysis of the Omicron variant. The findings revealed that Omicron has similar ACE2 binding affinity to Delta, but with an increased ability to evade neutralization by antibodies.
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Materials provided by University of British Columbia. Note: Content may be edited for style and length.

Researchers in Lund have discovered an antitoxin mechanism that seems to be able to neutralise hundreds of different toxins and may protect bacteria against virus attacks. The mechanism has been named Panacea, after the Greek goddess of medicine whose name has become synonymous with universal cure. The understanding of bacterial toxin and antitoxin mechanisms will be crucial for the future success of so-called phage therapy for the treatment of antibiotic resistance infections, the researchers say. The study has been published in PNAS.
So-called toxin-antitoxin systems, a kind of on-off switch in many bacterial DNA genomes, are increasingly being found to defend bacteria against attack by bacteriophages — viruses that infect bacteria. Activation of toxins allows bacterial populations to go into a kind of lockdown that limits growth and therefore the spread of the virus. As such, understanding the diversity, mechanisms and evolution of these systems is critical for the eventual success of phage therapy to treat antibiotic resistance infections. — Toxin-antitoxin pairs consist of a gene encoding a toxin that dramatically inhibits bacterial growth and an adjacent gene encoding an antitoxin that counteracts the toxic effect. It is like keeping a bottle of poison on a shelf next to a bottle of the antidote. While toxin-antitoxin pairs have been seen to evolve to associate with new toxins or antitoxins before, the scale of the neutralisation ability seen with Panacea — so called hyperpromiscuity — is unprecedented, explains researcher and group leader Gemma Atkinson at Lund University, who has led the study.
PhD student and co-first author Chayan Kumar Saha made a computer program for analysing the kinds of genes that are found next to each other in bacterial genomes. The team then used this tool to predict new antitoxin genes found next to some very potent toxins that they have previously worked on. “We were startled by the discovery that one particular antitoxin protein fold can be found in toxin-antitoxin-like arrangements with dozens of different kinds of toxins. Many of these toxins are new to science.”
The other first author Tatsuaki Kurata, Lund University, has confirmed experimentally that several of these systems are genuine toxins neutralized by the neighbouring antitoxin genes.
The study shows that what we know so far about the diversity of toxin-antitoxin systems probably is just the tip of the iceberg, and that there could be a range of similar systems that have gone under the radar until now. — As well as being important for understanding the weird and wonderful world of bacterial biochemistry, the discovery of new toxin-antitoxin systems is important for so-called phage therapy against antibiotic resistant infections. As bacteria have increasingly become resistant to antibiotics, other approaches are needed for eliminating infections.
The principle of phage therapy is to treat patients with cocktails of bacteriophages — viruses that infect bacteria — in order to kill the bacteria causing infection. However bacteria carry various defence systems to protect themselves from phages, and this includes toxin-antitoxin systems.
“Thus identifying toxin-antitoxin systems of pathogens may help us in the future design phage therapy that can counter this layer of defence,” explains Gemma Atkinson.
So, what is the next research step?
“We are now trying to find novel toxin-antitoxin systems on a universal scale, and understand their involvement in phage defence. We are also interested in possible biotechnological applications of toxin-antitoxin systems, given that these systems can be thought of as on-off switches of core aspects of bacterial biology. The full set of toxin-antitoxin systems could be a molecular toolbox for tweaking bacterial metabolism and controlling bacterial cell resources. This can be important in industrial and pharmaceutical manufacture situations where bacteria are used to produce molecules of interest.”
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Materials provided by Lund University. Original written by Agata Garpenlind. Note: Content may be edited for style and length.

Previous studies have shown how fasting can influence the immune system to improve different chronic inflammatory conditions, but little is known about how immune responses might determine a healthy metabolism. Since the liver is a central hub and regulator of metabolism, a group of researchers focused on understanding how liver cells and immune cells found in the liver communicate with each other in conditions of fasting. The study was a joint effort of Helmholtz Munich, Ulm University, the Technical University of Munich (TUM), the German Center for Diabetes Research (DZD), the Heidelberg University Hospital, and the University of Southern Denmark.
Immune activity is necessary for metabolic response to fasting
The researchers scanned the DNA of liver cells and immune cells, examining which parts of their DNA were active and which messenger-molecules were being released as a result. Their findings showed that these cells were communicating with one-another and highlighted the role of a molecule that is expressed in almost all the cells in our bodies, namely the glucocorticoid receptor. “We discovered that in the immune cells, this receptor in particular allowed the crosstalk between the cell types during fasting. By deleting the receptor only in the immune cells, we saw a breakdown of fasting signals in the liver cells. This means that the immune cells are able to directly influence the effect of fasting on our metabolism,” says Anne Loft from Helmholtz Munich.
Giorgio Caratti and Jan Tuckermann from the Ulm University add: “In fact, this is the first time we have seen this process under ‘healthy’ conditions. We knew that immune responses could influence our metabolism in an unhealthy setting, but this was new. It proves that a low level of immune activity, or inflammation, is necessary for a balanced metabolic response to fasting.”
“Voluntary fasting has been shown to be beneficial for the prevention of a number of human metabolic diseases, including type 2 diabetes and obesity. The increase in people suffering from not only these metabolic diseases is staggering, showing no signs of slowing down. Our findings serve to understand the molecular mechanisms behind these diseases and may ultimately lead to the development of effective fasting-based therapies,” says Stephan Herzig who led study at Helmholtz Munich.
Prof. Stephan Herzig is Director of the Helmholtz Diabetes Center at Helmholtz Munich. He holds the Chair for Molecular Metabolic Control at TUM and an Honorary Chair at Heidelberg University. Dr. Anne Loft is first author of the study at Helmholtz Munich. Both are part of the German Center for Diabetes Research (DZD). Dr. Giorgio Caratti from the Ulm University, Institute of Comparative Molecular Endocrinology is co-author of the study and works at Prof. Jan Tuckermann’s lab who led the study together with Stephan Herzig.
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Materials provided by Helmholtz Zentrum München – German Research Center for Environmental Health. Note: Content may be edited for style and length.

A study by Virginia Commonwealth University Massey Cancer Center researchers published in today’s print edition of Molecular Cancer Therapeutics shows that triplatin is effective against triple negative breast cancer, which is the most aggressive form of breast cancer and has few targeted therapies.
Triplatin, a 30-year-old drug, has faced a bumpy road on the path to Food and Drug Administration approval, but this study offers a new insight that could finally help to get it over the finish line.
The researchers found that about 40% of triple negative breast cancer cases had tumors rich in sugars called sulfated glycosaminoglycans (sGAG), which triplatin strongly binds to, causing the drug to accumulate inside cancer cells where it can do the most damage. The FDA-approved platinum-based drug carboplatin does the opposite, honing in on tumors with low sGAG levels and taking those out instead.
This result suggests that clinical trials revisiting triplatin can focus on patients with high sGAG levels to set the drug up for success, rather than diluting any positive effects among a mixed pool of patients.
“It’s very important that we have some idea of how the drug works so we can only treat those that will be most likely to respond,” said study co-senior author Nicholas Farrell, Ph.D., professor of chemistry at Virginia Commonwealth University. “Now, we have a new perspective.”
Triplatin originated in Farrell’s lab and was patented in the mid-1990s. In the 2000s, the drug underwent phase II clinical trials as a potential treatment for ovarian, lung and pancreatic cancer, but in all cases, the efficacy fell short of the threshold needed for FDA approval. So, phase III was scrapped and triplatin never made it to the clinic, despite the realization in hindsight that some of the participants who responded to the drug remained in remission for several years.

Scientists have revealed that protracted inflammation following COVID-19 is strongly linked to long-term changes in lung structure and function, according to a report published today in eLife.
The results suggest that monitoring people for markers of inflammation after infection with the SARS-CoV-2 virus could help identify those at risk of long-term lung problems and optimise follow-up care.
Although a vast majority of COVID-19 patients display mild disease, a significant proportion reports lingering or recurring clinical symptoms and full recovery can take several months to years.
“Symptoms lasting beyond 12 weeks are found in as many as 10% of COVID-19 patients and robust, resource-saving tools assessing people’s individual risk of lung complications are urgently needed,” says Thomas Sonnweber, a lung specialist at the Medical University of Innsbruck, Austria, and co-first author of the study alongside Piotr Tymoszuk. “We analysed the frequency of lung structure and function changes and persistent symptoms in patients six months after a COVID-19 diagnosis, to investigate whether there are clinical hallmarks that can predict their risk of developing long COVID.”
The researchers evaluated the recovery of 145 primarily hospitalised patients diagnosed with COVID-19 between March and June 2020 who took part in the Austrian clinical study called ‘Development of Interstitial Lung Disease in COVID-19’ (CovILD).
They retrospectively assessed patient characteristics during their acute COVID-19 infection and then performed follow-up investigations at 60, 100 and 180 days. At each visit, they assessed symptoms and physical performance using a questionnaire, and conducted lung function tests, blood tests and a chest scan.
Almost half (49%) of patients had persistent complaints six months after diagnosis, with the most common complaints being impaired physical performance (34.7% of patients), sleep disorders (27.1%) and breathlessness on exertion (22.8%). Although the frequency of these symptoms declined as time passed, they were slower to resolve towards the end of the convalescence period, at the 100-day and 180-day follow-up visits.
Six months after diagnosis, a third of patients (33.6%) had impaired lung function and almost half of patients (48.5%) had chest scans showing structural lung abnormalities, with one in five patients (19.4%) having moderate-to-severe lung alterations.
To identify risk factors associated with these long-term problems, the team used machine learning algorithms to look for patterns of clinical features in the patients who had long COVID symptoms. They found that risk factors linked to severe and critical COVID-19 infection — namely being male, having long-term conditions such as high blood pressure, and high anti-SARS-CoV-2 antibody levels — were also linked to long-term symptom persistence. But in addition to these factors, elevated markers of inflammation — both body-wide and within blood vessels — were also associated with long-term lung abnormalities.
The team then tested if algorithms using these risk factors could predict COVID outcomes in a different group of patients. They found that although the inflammation markers predicted who would develop lung structure abnormalities, they could not accurately predict who would develop lung function problems or other symptoms such as breathlessness. This suggests that even if patients have detectable changes to their lungs 60 days after diagnosis, this may not manifest as symptoms or changes in lung function yet, but could still lead to problems later.
The algorithms need to be validated in larger groups of patients with COVID-19 before they can be reliably used to predict long-term COVID-19 outcomes. To this end, the authors have published their findings as an open-source risk assessment tool for other researchers to use.
“In our study group of patients, we found a high frequency of structural and functional lung abnormalities and persistent symptoms six months after a COVID-19 diagnosis, and a recovery trajectory that slowed after three months,” concludes Judith Löffler-Ragg, a lung specialist at the Medical University of Innsbruck, and co-senior author of the study alongside Ivan Tancevski. “Our risk models revealed a set of clinical measurements linked to lengthened recovery, independent to the severity of infection, which include known inflammatory markers. We hope that these could be used to identify those at risk of persistent lung problems and optimise their care to prevent long-term disability.”
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Materials provided by eLife. Note: Content may be edited for style and length.

An online symptom management tool that harnesses the problem-solving benefits of expressive writing could help women with ovarian cancer better manage complex symptoms, according to a new study led by a University of Pittsburgh and UPMC nurse-scientist.
Published today in the Journal of Clinical Oncology, the study found that patients who used nurse-led and self-directed versions of the tool reported a better sense of control over symptoms compared to enhanced usual care.
“Women with ovarian cancer experience an average of 14 concurrent symptoms, so symptom management is very complex. It can be overwhelming for patients and challenging for providers, who may not have time to address these symptoms in a typical 15-minute appointment,” said lead author Heidi Donovan, Ph.D., R.N., professor of health and community systems in Pitt’s School of Nursing and obstetrics, gynecology and reproductive services in the School of Medicine. “That’s why we developed a symptom management approach outside of a normal clinical setting, from the comfort of a woman’s own home.”
According to Donovan, ovarian cancer is a “low incidence, high impact cancer.” In 2022, about 20,000 women will be diagnosed with ovarian cancer in the U.S., and more than 12,000 will die. For many patients who are treated successfully, the cancer recurs after two to three years.
“There’s a vast difference in quality of life between patients who manage symptoms successfully and those who don’t, both throughout chemotherapy and afterwards,” said Donovan, who is also director of the Gynecologic Oncology Family CARE Center at UPMC Magee-Womens Hospital. “Effective symptom management requires that patients follow directions from providers but also be willing to communicate, make adjustments and try new strategies.”
Donovan and her team developed a new symptom management approach called Written Representational Intervention to Ease Symptoms, or WRITE Symptoms, which guides patients to reflect on how they experience a symptom: what causes it, what makes it worse, how it feels, how it impacts their daily life and how they’ve tried to manage it.