Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health
The composition of microbiota found in the gut influences how susceptible mice are to respiratory virus infections and the severity of these infections, according to Georgia State University researchers. The findings, published in the journal Cell Host & Microbe, report that segmented filamentous bacteria, a bacterial species found in the intestines, protected mice against influenza virus infection when these bacteria were either naturally acquired or administered.
This protection against infection also applied to respiratory syncytial virus (RSV) and severe acute SARS-CoV-2. To maintain this protection, the study noted that segmented filamentous bacteria required immune cells in the lungs called basally resident alveolar macrophages.
In this study, the researchers investigated how differences in specific microbial species can impact outcomes of respiratory virus infections and how they might do so, which hasn’t been well defined previously.
They studied mice with discrete microbiome differences and mice differing in only the presence or absence of segmented filamentous bacteria.
Viral titers in the lung were measured several days after infection and varied significantly depending on the nature of the microbiome of the different animal groups.
“These findings uncover complex interactions that mechanistically link the intestinal microbiota with the functionality of basally resident alveolar macrophages and severity of respiratory virus infection,” said Dr. Andrew Gewirtz, co-senior author of the study and Regents’ Professor in the Institute for Biomedical Sciences at Georgia State.
The study found that in segmented filamentous bacteria-negative mice, basally resident alveolar macrophages were quickly depleted as respiratory virus infection progressed.
However, in segmented filamentous bacteria-colonised mice, basally resident alveolar macrophages were altered to resist influenza virus infection depletion and inflammatory signaling.
The basally resident alveolar macrophages disabled influenza virus, in large part by activating a component of the immune system referred to as the complement system.
“We find it remarkable that the presence of a single common commensal bacterial species, amidst the thousands of different microbial species that inhabit the mouse gut, had such strong impacts in respiratory virus infection models and that such impacts were largely attributable to reprogramming of basally resident alveolar macrophages,” said D. Richard Plemper, co-senior author of the study, Regents’ Professor and director of the Center for Translational Antiviral Research at Georgia State.
“If applicable to human infections, these findings will have major implications for the future risk assessment of a patient to advance to severe disease.”
“We find it highly unlikely that segmented filamentous bacteria is the only gut microbe capable of impacting the phenotype of alveolar macrophages, and consequently, proneness to respiratory virus infection,” Gewirtz said.
“Rather, we hypothesize that gut microbiota composition broadly influences proneness to respiratory virus infection. Microbiota mediated programming of basally resident alveolar macrophages may not only influence the severity of acute respiratory virus infection, but may also be a long-term post-respiratory virus infection health determinant.”
Photo by Towfiqu barbhuiya: https://www.pexels.com/photo/a-toothbrush-with-toothpaste-on-a-white-surface-12065623/
A new study by investigators from Brigham and Women’s Hospital examined whether daily toothbrushing among hospitalised patients is associated with lower rates of hospital-acquired pneumonia and other outcomes. Their analysis of 15 randomised clinical trials found that hospital-acquired pneumonia rates were lower among patients who received daily toothbrushing compared to those who did not. The results were especially compelling among patients on mechanical ventilation. Their results are published in JAMA Internal Medicine.
“The signal that we see here towards lower mortality is striking – it suggests that regular toothbrushing in the hospital may save lives,” said corresponding author Michael Klompas, MD, MPH, hospital epidemiologist and an infectious disease physician in the Department of Medicine at BWH and Professor of Population Medicine at Harvard Pilgrim Health Care Institute.
“It’s rare in the world of hospital preventative medicine to find something like this that is both effective and cheap. Instead of a new device or drug, our study indicates that something as simple as brushing teeth can make a big difference.”
Hospital-acquired pneumonia occurs when bacteria in the mouth enter a patient’s airways and infect their lungs.
Patients experiencing frailty or patients with a weakened immune system are particularly susceptible to developing hospital-acquired pneumonia during their hospital stay.
However, adopting a daily toothbrushing regimen can decrease the amount of bacteria in the mouth, potentially lowering the risk of hospital-acquired pneumonia from occurring.
The team conducted a systematic review and meta-analysis to determine the association between daily toothbrushing and hospital-acquired pneumonia.
Using a variety of databases, the researchers collected and analysed randomised clinical trials from around the world that compared the effect of regular oral care with toothbrushing versus oral care without toothbrushing on the occurrence of hospital-acquired pneumonia and other outcomes.
The team’s analysis found that daily toothbrushing was associated with a significantly lower risk for hospital-acquired pneumonia and ICU mortality.
In addition, the investigators identified that toothbrushing for patients in the ICU was associated with fewer days of mechanical ventilation and a shorter length of stay in the ICU.
Most of the studies in the team’s review explored the role of a teeth-cleaning regimen in adults in the ICU.
Only two of the 15 studies included in the authors’ analysis evaluated the impact of toothbrushing in non-ventilated patients.
The researchers are hopeful that the protective effect of toothbrushing will extend to non-ICU patients but additional studies focusing on this population are needed to clarify if in fact this is the case.
“The findings from our study emphasise the importance of implementing an oral health routine that includes toothbrushing for hospitalised patients. Our hope is that our study will help catalyse policies and programs to assure that hospitalised patients regularly brush their teeth. If a patient cannot perform the task themselves, we recommend a member of the patient’s care team assist,” said Klompas.
Mayo Clinic researchers mapped how the measles virus mutated and spread in the brain of a person who succumbed to a rare, lethal brain disease. New cases of this disease, which is a complication of the measles virus, may occur as measles re-emerges among the unvaccinated, say researchers.
Using the latest tools in genetic sequencing, researchers at Mayo Clinic reconstructed how a collective of viral genomes colonised a human brain.
The virus acquired distinct mutations that drove the spread of the virus from the frontal cortex outward.
The highly contagious measles virus infects the upper respiratory tract where it uses the trachea as a trampoline to launch and spread through droplets dispersed when an infected person coughs or sneezes.
Dr Cattaneo pioneered studies on how the measles virus spreads throughout the body. He first began to study the measles virus about 40 years ago and was fascinated by the rare, lethal brain disease called subacute sclerosing panencephalitis (SSPE), which occurs in about 1 in every 10 000 measles cases.
It can take about five to 10 years after the initial infection for the measles virus to mutate and spread throughout the brain.
Symptoms of this progressive neurological disease include memory loss, seizures and immobility.
Dr. Cattaneo studied SSPE for several years until the lethal disease nearly disappeared as more people were vaccinated against measles. But now, measles is resurging due to vaccine hesitancy and missed vaccinations.
During the COVID pandemic, millions of children missed receiving their measles vaccinations, which has resulted in an estimated 18% increase in measles cases and 43% increase in death from measles in 2021 compared to 2022 worldwide, according to a recent Centers for Disease Control and Prevention (CDC) report.
“We suspect SSPE cases will rise again as well. This is sad because this horrible disease can be prevented by vaccination. But now we are in the position to study SSPE with modern, genetic sequencing technology and learn more about it,” says Iris Yousaf, co-lead author of the study and a fifth-year Ph.D. candidate at Mayo Clinic Graduate School of Biomedical Sciences.
Dr Cattaneo and Yousaf had a unique research opportunity through a collaboration with the CDC. They studied the brain of a person who had contracted measles as a child and had succumbed to SSPE years later as an adult.
They investigated 15 specimens from different regions of the brain and conducted genetic sequencing on each region to piece together the puzzle of how the measles virus mutated and spread.
The researchers discovered that, after the measles virus entered the brain, its genome began to mutate in harmful ways over successive generations, creating a population of varied genomes.
“In this population, two specific genomes had a combination of characteristics that worked together to promote virus spread from the initial location of the infection – the frontal cortex of the brain – out to colonise the entire organ,” says Dr Cattaneo.
The next steps in this research are to understand how specific mutations favour virus spread in the brain. These studies will be done in cultivated brain cells brain organoids. This knowledge may help in creating effective antiviral drugs to combat virus spread in the brain. However, pharmacological intervention in advanced disease stages is challenging, and preventing SSPE through measles vaccination remains the best method.
It has long been known that people with diabetes are at a substantially increased risk of developing severe lung disease if they become infected with viruses such as influenza, as well as other pathogens. When the COVID-19 pandemic started in early 2020, it became even more important to understand this mysterious phenomenon. It became clear that people with diabetes were at a significantly higher risk of coming down with severe, even fatal, lung disease after developing severe COVID, but no one understood why. In fact, some 35% of the pandemic’s COVID mortalities had diabetes.
Now, research conducted at the Weizmann Institute of Science and published in Nature has revealed how, in diabetics, high levels of blood sugar disrupt the function of key cell subsets in the lungs that regulate the immune response. It also identifies a potential strategy for reversing this susceptibility and saving lives.
Prof. Eran Elinav‘s team in his lab at Weizmann, headed by Drs. Samuel Nobs, Aleksandra Kolodziejczyk and Suhaib K. Abdeen, subjected multiple mouse models of types 1 and 2 diabetes to a variety of viral lung infections. Just as in diabetic humans, in all these models the diabetic mice developed a severe, fatal lung infection following exposure to lung pathogens such as influenza. The immune reaction, which in nondiabetics eliminates the infection and drives tissue healing, was severely impaired in the diabetic mice, leading to uncontrolled infection, lung damage and eventual death.
Next, to decode the basis of this heightened risk, the team performed an evaluation of gene expression on the level of individual cells, in more than 150 000 single lung cells of infected diabetic and nondiabetic mice. The researchers also performed an extensive array of experiments involving immune and metabolic mechanisms, as well as an in-depth assessment of immune cell gene expression in infected diabetic mice. In the diabetic mice they identified a dysfunction of certain lung dendritic cells, the immune cells that orchestrate a targeted immune response against pathogenic infection. “High blood sugar levels severely disrupt certain subsets of dendritic cells in the lung, preventing these gatekeepers from sending the molecular messages that activate the critically important immune response,” says Nobs, postdoctoral fellow and study first author. “As a result, the infection rages on, uncontrolled.”
Next, they explored ways to prevent the harmful effects of hyperglycaemia in lung dendritic cells, as a means of lowering the infection’s risk in diabetic animals. Indeed, tight control of glycaemic levels by insulin supplementation prompted the dendritic cells to regain their capacity to generate a protective immune response that could prevent the cascade of events leading to a severe, life-threatening viral lung infection. Alternatively, administration of small molecules reversing the sugar-induced regulatory impairment corrected the dendritic cells’ dysfunction and enabled them to generate a protective immune response despite the presence of hyperglycaemia.
“Correcting blood sugar levels, or using drugs to reverse the gene regulatory impairment induced by high sugar, enabled our team to get the dendritic cells’ function back to normal,” says Abdeen, a senior intern who co-supervised the study. “This was very exciting because it means that it might be possible to block diabetes-induced susceptibility to viral lung infections and their devastating consequences.”
Lung tissue of a diabetic mouse (right) contains fewer immune cells (small purple dots) than that of a non-diabetic animal (left)
With over 500 million people around the world affected by diabetes, and with diabetes incidence expected to rise over the next decades, the new research has significant, promising clinical implications.
“Our findings provide, for the first time, an explanation as to why diabetics are more susceptible to respiratory infection,” Elinav says. “Controlling sugar levels may make it possible to reduce this pronounced diabetes-associated risk. In diabetic patients whose sugar levels are not easily normalized, small molecule drugs may correct the gene alterations caused by high sugar levels, potentially alleviating or even preventing severe lung infection. Local administration of such treatments by inhalation may minimize adverse effects while enhancing effectiveness, and merits future human clinical testing.”
A European study showed that 92% of patients using the biologic therapy benralizumab could safely reduce inhaled steroid dose and more than 60% could cease entirely. The results, published in The Lancet, could be transformative for severe asthma patients by minimising or eliminating the unpleasant, and often serious, side effects of inhaled steroids.
These include osteoporosis which leads to increased risk of fractures, diabetes and cataracts.
Around 3 to 5% of the 300 million people with asthma worldwide have severe asthma. This leads to daily symptoms of breathlessness, chest tightness and cough, along with repeated asthma attacks which require frequent hospitalisation.
The SHAMAL study was led by Professor David Jackson, head of the Severe Asthma Centre at Guy’s and St Thomas’ and Professor of Respiratory Medicine at King’s College London.
Professor Jackson said: “Biological therapies such as benralizumab have revolutionised severe asthma care in many ways, and the results of this study show for the first time that steroid related harm can be avoided for the majority of patients using this therapy.”
The monoclonal antibody benralizumab targets interleukin-5, reducing eosinophil count, which is elevated in the airway of patients with severe asthma and is critically involved in the development of asthma attacks.
Benralizumab is injected every four to eight weeks.
The SHAMAL study took place across 22 sites in the UK, France, Italy and Germany.
The 208 patients were randomly assigned to taper their high dose inhaled steroid by varying amounts over 32 weeks, followed by a 16 week maintenance period.
Approximately 90% of patients experienced no worsening of asthma symptoms and remained free of any exacerbations throughout the 48 week study.
Similar studies to SHAMAL will be necessary before firm recommendations can be made regarding the safety and efficacy of reducing or eliminating high dose steroid use with other biologic therapies.
The World Health Organization (WHO) noted an upsurge of unidentified pneumonia-like respiratory illnesses among children in Northern China, and asked China for more information. This is significant as previous outbreaks of severe respiratory illnesses have started out in this fashion, but such WHO requests for more information on disease clusters are routine as part of its monitoring. No “unusual or novel pathogens” have been found, according to China, which attributed it to an increase in multiple pathogens and the lifting of COVID restrictions.
Earlier this month, China’s National Health Commission reported a nationwide increase in respiratory disease incidence, mostly among children. This increase was attributed to lifting of COVID restrictions and the arrival of the cold season, and due to circulating known pathogens including Mycoplasma pneumonia and RSV, which are known to affect children more than adults.
On 22 November 2023, the WHO identified media and ProMED reports about clusters of undiagnosed pneumonia in children’s hospitals in Beijing, Liaoning and other places in China. The WHO requested from China additional epidemiologic and clinical information, as well as lab results from these cases and data about recent trends in circulating respiratory pathogens.
The WHO held a teleconference with Chinese health authorities and received data indicating an increase in outpatient consultations and hospital admissions of children due to Mycoplasmapneumoniae pneumonia since May, and RSV, adenovirus and influenza virus since October. Some of these increases are earlier in the season than usual, but not unexpected given the lifting of COVID restrictions, as similarly experienced in other countries. No changes in the disease presentation were reported by the Chinese health authorities, who said no unusual or novel pathogens or unusual clinical presentations had been detected, but only the general increase in respiratory illnesses by known pathogens. Local hospitals had not been overloaded by new cases.
Risk assessment
In the current outbreak of respiratory illness, the reported symptoms are common to several respiratory diseases and, as of now, at the present time, Chinese surveillance and hospital systems report that the clinical manifestations are caused by known pathogens in circulation. M. pneumoniae is a common respiratory pathogen and a common cause of paediatric pneumonia, and is readily treated with antibiotics.
China has stepped up its influenza-like illness (ILI) and severe acute respiratory infections (SARI) sentinel surveillance system since mid-October, including for M. pneumoniae.
There is limited detailed information available to fully characterize the overall risk of these reported cases of respiratory illness in children. However, due to the arrival of the winter season, the increasing trend in respiratory illnesses is expected; co-circulation of respiratory viruses may increase burden on health care facilities.
According to surveillance data reported to WHO’s FluNet and published by the National Influenza Centre in China, ILI was above usual levels for this time of year and increasing in the northern provinces. Influenza detections were predominantly A(H3N2) and B/Victoria lineage viruses.
WHO advice
The WHO advice was for people in China to take measures against respiratory illnesses, including vaccines, masking and social distancing. It also does not recommend any specific measures for travellers to China.
Scientists have uncovered a group of T cells that may drive severe asthma, which gather in the lungs and seem most harmful in men who develop asthma in later life. The new research, published in MED, suggests asthma patients with these cells in their lungs may be more likely to have hard-to-treat, and potentially fatal, asthma attacks. These cells do not respond to the usual general therapy for asthma patients.
The scientists, from the University of Southampton and La Jolla Institute for Immunology (LJI), in California, uncovered these T cells, called ‘cytotoxic CD4+ tissue-resident memory T cells’, thanks to volunteers enrolled in the NHS clinic-based WATCH study. It follows hundreds of asthma patients of different ages, sexes, and disease severities. By following patients over many years, and analysing their immune cell populations, researchers are making new connections between asthma symptoms and immune cell activity.
“If you are male and you develop asthma after age 40, there’s a high chance this T cell population is in your lungs,” says LJI Research Assistant Professor Gregory Seumois, who co-led the study with LJI Professor Pandurangan Vijayanand.
“Once you understand the role of cells like these T cells better, you can start to develop treatments that target those cells,” says WATCH study director Dr Ramesh Kurukulaaratchy, Associate Professor at the University of Southampton and researcher at the NIHR Southampton Biomedical Research Centre.
Scientists now hope to learn more about these cells and their role in asthma development in order to develop personalised therapies for asthma patients.
How harmful T cells drive asthma
The ‘memory’ T cells help protect the body from viruses and bacteria it has encountered before, but the same T cell memory is a big problem for asthma patients. Their misguided T cells see harmless molecules, such as pollen, and produce a dangerous inflammatory response.
Men who developed asthma later in life had an overwhelming number of these potentially harmful T cells. Their lungs should have been home to a diverse bunch of CD4+ T cell types but, in this group, more than 65% of their cells were cytotoxic CD4+ tissue-resident memory T cells.
Personalised asthma treatments
Single-cell RNA sequencing by LJI scientists provides a ‘biomarker’ to help detect cytotoxic CD4+ tissue-resident memory T cells in more patients going forward.
Finding this biomarker represents a “paradigm shift” in asthma research, says Dr Kurukulaaratchy. Before now, scientists and clinicians separated asthma patients into just two groups: ‘T2 high’ and T2 low’. In a study published earlier this year, the research team showed the importance of drilling down to identify many more asthma patient subgroups; their analysis reveals that 93% of WATCH subjects with severe asthma were in the T2 high category.
Study co-author Professor Hasan Arshad, Chair in Allergy and Clinical Immunology at the University of Southampton, researcher at the NIHR Southampton Biomedical Research Centre, and Director of The David Hide Asthma and Allergy Research Centre, Isle of Wight says: “We have to think of severe asthma as having different subtypes, and the treatment has to be tailored according to these subtypes because one size does not fit all.”
The researchers now want to use sequencing tools and other techniques to discover additional biomarkers and asthma patient subtypes.
In a pivotal case for access to affordable medicines in South Africa, the Treatment Action Campaign (TAC) and Doctors Without Borders (MSF) Southern Africa – represented by SECTION27 – earlier this year came together to help champion access to lifesaving new cystic fibrosis treatments.
Cheri Nel, a South African woman living with cystic fibrosis, and the Cystic Fibrosis Association started legal action against Vertex Pharmaceuticals earlier this year, challenging Vertex’s monopoly on the treatments. The TAC and MSF approached the court to be joined as amici curiae. Vertex, an American pharmaceutical company, holds the patents for both Trikafta and Kalydeco – medicines that have the potential to significantly improve the lives of cystic fibrosis patients. However, at a price of US $311 000 per year per patient in the United States (over R5 million), it is out of reach for most people living with cystic fibrosis.
The court application is for a compulsory licence, which, if granted, will mean another manufacturer of generics for Trikafta and Kalydeco would be permitted to enter the South African market. In this case, it is likely that competition between manufacturers would affect the price of this medicine, thus making it more accessible. A compulsory licence allows the holder of the license to produce a patented product without the patent holder’s consent.
Johannesburg-based investment banker Cheri Nel is the driving force behind a court case that may result in dramatically expanded access to life-changing new cystic fibrosis (CF) medicines. PHOTO: Supplied
Spotlight previously reported that Nel’s lawyers argued that by failing to register or supply their CF medicines in South Africa, make them available in South Africa at reasonable prices, or license other companies to supply the medicines, Vertex is abusing its patents. They further argued that Vertex’s actions are violating the Constitutional rights of people with cystic fibrosis in South Africa, including the right to health care. (Spotlight previously reported on the issue here, here, and here.)
Cystic fibrosis is a devastating multi-system illness known for causing frequent and severe lung infections, liver and pancreatic damage, lung failure, and can result in the potential need for lung transplants even in children from as young as two years old.
This case will set an important precedent that can influence access to medicines not only in South Africa but around the world. The involvement of SECTION27, where I work, underscores the broader issue of affordable access to medicines and the impact of intellectual property on healthcare access.
At present, MSF and TAC are awaiting the court’s decision to be admitted as friends of the court, while in the main application, the respondent (Vertex) has filed answering affidavits.
And while the clock is ticking in the courts, many families in South Africa are waiting and holding on to the glimmer of hope access to this medicine represents. For many who live with cystic fibrosis, a successful outcome of Nel and the Cystic Fibrosis Association’s application will mean a life where they can breathe easier.
Among those waiting is 6-year-old Janco Koorts.
A journey of hope
His mother, Tanya Koorts, says living with cystic fibrosis is like fighting every day for every breath. She says Janco had been diagnosed with cystic fibrosis at the age of two. She has since been on a mission to raise awareness about this life-threatening disease. It is hope, her family, and the support from the cystic fibrosis community that has kept her going, she says.
Reflecting on the start of their journey in the Northern Cape, she says, “The knowledge about cystic fibrosis is very little. We were lucky that Dr Jooste at the Kimberly public hospital diagnosed him so early on. After that, he sent us to the Red Cross Hospital in Cape Town and so our long journey of hope started.”
Later in a new job in a new city, the Koorts began again in Pretoria. They started Janco’s treatment at the Steve Biko Academic Hospital and then moved to the Charlotte Maxeke Johannesburg Academic Hospital.
“They don’t have much, but they do everything they can there to help. They also don’t have a lot of support but the people at Charlotte Maxeke helped Janco on his journey to stay breathing,” Koorts says, applauding the public health system.
Janco now has comprehensive medical aid which covers his monthly R48 000 medication bill and Koorts says she can now “breathe easier”. That, however, is just a fraction of the cost of living with cystic fibrosis.
When the Koorts family heard about Trixacar, a generic version of Trikafta, it only strengthened their resolve to save Janco’s life. The patent rights registered by Vertex Pharmaceuticals in South Africa, however, do not allow for the import of Trixacar. Trixacar is produced by the pharmaceutical company Gador in Argentina. Koorts will thus have to travel to Argentina to buy the medicine. This will cost about R400 000 to cover the travel costs and six boxes of Trixacar that will last six months, she says. (You can help the family fund this by donating here.)
‘a thief of joy’
Apart from the financial burden, having a young child with cystic fibrosis has affected the Koorts family mentally and emotionally.
“Cystic fibrosis is a thief of joy. Nobody speaks about fighting to save someone’s life,” says Koorts.
She says her family had to adjust to some of the social changes in their surroundings as well.
“At school, he has to fight for himself to stay alive. If we go to a restaurant and there are people smoking, it affects him and we have to move. So, as much as we have tried to give Janco a normal childhood, these social aspects will always hinder progress, and he is always reminded that he is sick. But I live in hope and so does he.”
In terms of her family relationships, Tanya says that her other children are healthy and for them to see their baby brother suffering every day hurts them.
“It’s painful as parents. Janco needs all the attention. I can’t go to a parent’s evening for my other kids. It’s difficult,” Koorts says.
She says she is proud of Janco.
“My child doesn’t know that he is dying. We fight every day so that Janco can have just one more breath.”
And that is ultimately what it is all about. From one perspective the exchange of documents in the High Court may seem abstract and full of legal technicalities. But let there be no doubt, for kids like Janco it is literally their futures that are being decided.
*Adams is a communications officer at SECTION27.
NOTE: This opinion piece was written by a staff member of SECTION27. Spotlight is published by SECTION27 and the TAC, but is editorially independent – an independence that the editors guard jealously. The views expressed in this piece are not necessarily those of Spotlight.
A new study from Aarhus University has shown that young people with mild asthma can experience inflammation and irritation from candles as well as cooking fumes. The results, published in Particle and Fibre Toxicology, suggest that asthma sufferers should try and reduce exposure, for example by opening kitchen windows while cooking.
For this randomised controlled double-blind exposure study, exposed 36 young asthmatics to three different exposures in the climate chambers at Aarhus University. They were exposed to emissions from cooking, emissions from burning candles and finally clean air. Each time, the participants were exposed for five hours under highly controlled conditions. Particles and gases were measured during exposures, and participants reported symptoms related to irritation and general well-being. Biomarkers in relation to airway and systemic inflammatory changes were assessed before exposure, immediately after exposure and again the next morning.
Karin Rosenkilde Laursen, a postdoc at the university’s Department of Public Health and co-author of the study, says:
“Our study shows that indoor air pollution caused by fumes from cooking and burning candles can lead to adverse health effects such as irritation and inflammation in young individuals with mild asthma. Among other things, we’ve found indications of DNA damage and signs of inflammation in the blood.”
When ovens are turned, pans put on the hob, or candles are lit, particulate matter and gases are produced, which can be inhaled. Previous studies have shown that these particles and gases can be detrimental to health. What sets this study apart is that the researchers have focused on the effects on young individuals with mild asthma, aged between 18 and 25, says Karin Rosenkilde Laursen:
“In the study, we observed that even very young individuals with mild asthma can experience discomfort and adverse effects if the room is not adequately ventilated during cooking or when burning candles. Young people are generally fitter and more resilient than older and middle-aged individuals. Therefore, it is concerning that we observed a significant impact from the particles on this particularly young age group.”
But not only people diagnosed with asthma need to keep an eye on the indoor climate, she says.
“Even though the study focused on young asthmatics, its findings are interesting and relevant for all of us. Winter is approaching, a time when we tend to light many candles and perhaps are less likely to open doors and windows while cooking. By prioritising a healthier indoor climate, even when we’re cosying up indoors, we may be able to help reduce the incidence of serious lung and cardiovascular diseases, as well as cancer.”
Karin Rosenkilde Laursen plans to follow up this study with another examining how emissions from cooking and candles affect healthy adults.
A new study suggests boys who smoke in their early teens risk damaging the genes of their future children, increasing their chances of developing asthma, obesity and low lung function.
This research, published in Clinical Epigenetics, is the first human study to reveal the biological mechanism behind the impact of fathers’ early teenage smoking on their children.
Researchers from the University of Southampton and the University of Bergen in Norway investigated the epigenetic profiles of 875 people, aged 7 to 50, and the smoking behaviours of their fathers.
They found epigenetic changes at 19 sites mapped to 14 genes in the children of fathers who smoked before the age of 15. These changes in the way DNA is packaged in cells (methylation) regulate gene expression (switching them on and off) and are associated with asthma, obesity and wheezing.
“Our studies in the large international RHINESSA, RHINE and ECRHS studies have shown that the health of future generations depends on the actions and decisions made by young people today – long before they are parents – in particular for boys in early puberty and mothers/grandmothers both pre-pregnancy and during pregnancy,” says Professor Cecilie Svanes from the University of Bergen and Research Director of the RHINESSA study. “It is really exciting that we have now been able to identify a mechanism that explains our observations in the cohorts.”
‘Unique markers’
“Changes in epigenetic markers were much more pronounced in children whose fathers started smoking during puberty than those whose fathers had started smoking at any time before conception,” says co-lead author of the paper Dr Negusse Kitaba, Research Fellow at the University of Southampton. “Early puberty may represent a critical window of physiological changes in boys. This is when the stem cells are being established which will make sperm for the rest of their lives.”
The team also compared the paternal preconception smoking profiles with people who smoked themselves and those whose mothers smoked before conception.
“Interestingly, we found that 16 of the 19 markers associated with fathers’ teenage smoking had not previously been linked to maternal or personal smoking,” says Dr Gerd Toril Mørkve Knudsen from the University of Bergen and co-lead author of the study. “This suggests these new methylation biomarkers may be unique to children whose fathers have been exposed to smoking in early puberty.”
Teenage vaping ‘deeply worrying’
The number of young people smoking has fallen in the UK in recent years. But co-author Professor John Holloway, from the University of Southampton and the NIHR Southampton Biomedical Research Centre, is concerned about children taking up vaping.
“Some animal studies suggest that nicotine may be the substance in cigarette smoke that is driving epigenetic changes in offspring,” says Professor Holloway. “So it’s deeply worrying that teenagers today, especially teenage boys, are now being exposed to very high levels of nicotine through vaping.
“The evidence from this study comes from people whose fathers smoked as teenagers in the 60s and 70s, when smoking tobacco was much more common. We can’t definitely be sure vaping will have similar effects across generations, but we shouldn’t wait a couple of generations to prove what impact teenage vaping might have. We need to act now.”
The new findings have significant implications for public health. They suggest a failure to address harmful exposures in young teenagers today could damage the respiratory health of future generations, further entrenching health inequalities for decades to come.
