̽��ֱ�� of Cambridge - Clare Bryant

When inflammation goes too far

lkm37 — Tue, 11 Mar 2025 10:05:23 +0000

Clare Bryant, Professor of Innate Immunity, is a molecular detective. Clare allows us to see how inflammation functions across species, and when our defence systems go too far.

Cambridge initiative to address risks of future engineered pandemics

cjb250 — Thu, 27 Feb 2025 08:00:39 +0000

These are some of the questions being addressed by a new initiative launched today at the ̽��ֱ�� of Cambridge, which seeks to address the urgent challenge of managing the risks of future engineered pandemics.

̽��ֱ��Engineered Pandemics Risk Management Programme aims to understand the social and biological factors that might drive an engineered pandemic and to make a major contribution to building the UK’s capability for managing these risks. It will build a network of experts from academia, government, and industry to tackle the problem.

Increased security threats from state and non-state actors, combined with increased urbanisation and global mobility, means the threat of deliberate pathogen release must be taken seriously as must other intertwined aspects of pandemic risk such as mis- and disinformation, the erosion of trust in a number of institutions and an increasingly volatile geopolitical context. Further potential risks are posed by recent developments in gene-editing tools and artificial intelligence, which have rapidly advanced technological capability that may make it easier to engineer potential pandemic pathogens.

Professor Clare Bryant from the Department of Medicine at the ̽��ֱ�� of Cambridge said: “There is a great opportunity to take a joined-up approach to managing the risks posed by engineered pandemics. We need experts and agencies across the spectrum to work together to develop a better understanding of who or what might drive such events and what their likely impact would be. And we need evidence-informed policies and networks in place that would help us respond to – or better still, prevent – such an eventuality.”

̽��ֱ��aims of the Engineered Pandemics Risk Management Programme are:
To develop the conceptual underpinnings for the risk management of engineered pandemics based on interdisciplinary research
To support the capability of the UK’s engineered pandemic risk policy and practice, including building and maintaining networks that connect government, academia and industry.
To strengthen the international networks that will support this work globally

There are four main strands of work:

Social determinants of engineered pandemic threat

This strand will look at the actors who have the potential to engineer harmful pathogens, either deliberately or accidentally. It will ask questions such as: What could motivate bioterrorism in the coming decades? Who might the relevant actors be? What are the kinds of engineered pandemic that someone might want to create?

Dr Rob Doubleday, Executive Director of the Centre for Science and Policy at the ̽��ֱ�� of Cambridge, said: “ ̽��ֱ��common narrative is that there’s a wide range of potential actors out there who want to create bioweapons but don’t yet have the technical means. But in fact, there’s been very little work to really understand who these people might be, and their relationship to emerging technology. To explore these questions, we need a broad network including social scientists, biosecurity researchers, criminologists, experts in geopolitics and counterterrorism.”

̽��ֱ��strand will also look at the governance of scientific research in areas that may facilitate an engineered pandemic, whether unwittingly or maliciously, aiming to deliver a policy framework that enables freedom of intellectual research while managing real and apparent risk in infectious disease research.

Professor Bryant said: “As scientists, we’re largely responsible for policing our own work and ensuring integrity, trustworthiness and transparency, and for considering the consequences of new knowledge and how it might be used. But with the rapid progress of genomic technologies and AI, self-regulation becomes more difficult to manage. We need to find governance frameworks that balance essential scientific progress with its potential misapplication.”

Biological determinants of engineered pandemic threat

Recognising that the most likely cause of an engineered pandemic would be the deliberate release of a naturally-occurring pathogen – viral or bacterial, for example – rather than a man-made pathogen, this strand aims to understand what might make a particular pathogen infectious and how our immune systems respond to infection. This knowledge will allow researchers to screen currently available drugs to prevent or treat infection and to design vaccines quickly should a pandemic occur.

Modelling threats and risk management of engineered pandemics

̽��ֱ��Covid-19 pandemic highlighted practical problems of dealing with pandemic infections, from the provision of personal protective equipment (PPE) to ensuring a sufficient supply of vaccine doses and availability of key medications. Modelling the potential requirements of a pandemic, how they could be delivered, how ventilation systems could be modiﬁed, what biosafety measures could be taken, for example, are all key challenges for managing any form of pandemic. This strand will address how existing modelling approaches would need to be adapted for a range of plausible engineered pandemics.

Policy innovation challenges

Working with the policy community, the Cambridge team will co-create research that directly addresses policy needs and involves policy makers. It will support policy makers in experimenting with more joined-up approaches through testing, learning and adapting solutions developed in partnership.

̽��ֱ��Engineered Pandemics Risk Management Programme is supported by a £5.25 million donation to the Centre for Research in the Arts, Humanities and Social Sciences (CRASSH) at the ̽��ֱ�� of Cambridge. ̽��ֱ��team intends it to form a central component of a future Pandemic Risk Management Centre, for which it is now fundraising.

Professor Joanna Page, Director of CRASSH, said: “Cambridge has strengths across a broad range of disciplines – from genetics and immunology to mathematical modelling to existential risk and policy engagement – that can make a much-needed initiative such as this a success.”

To find out more, visit the Engineered Pandemic Risk Management website.

Covid-19 showed us how vulnerable the world is to pandemics – but what if the next pandemic were somehow engineered? How would the world respond – and could we stop it happening in the first place?

There is a great opportunity to take a joined-up approach to managing the risks posed by engineered pandemics

Clare Bryant

Martin Sanchez

Illustration showing global pandemic spread

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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Scientists identify how fasting may protect against inflammation

cjb250 — Tue, 30 Jan 2024 09:55:30 +0000

In research published in Cell Reports, the team describes how fasting raises levels of a chemical in the blood known as arachidonic acid, which inhibits inflammation. ̽��ֱ��researchers say it may also help explain some of the beneficial effects of drugs such as aspirin.

Scientists have known for some time that our diet – particular a high-calorie Western diet – can increase our risk of diseases including obesity, type 2 diabetes and heart disease, which are linked to chronic inflammation in the body.

Inflammation is our body’s natural response to injury or infection, but this process can be triggered by other mechanisms, including by the so-called ‘inflammasome’, which acts like an alarm within our body’s cells, triggering inflammation to help protect our body when it senses damage. But the inflammasome can trigger inflammation in unintentional ways – one of its functions is to destroy unwanted cells, which can result in the release of the cell’s contents into the body, where they trigger inflammation.

Professor Clare Bryant from the Department of Medicine at the ̽��ֱ�� of Cambridge said: “We’re very interested in trying to understand the causes of chronic inflammation in the context of many human diseases, and in particular the role of the inflammasome.

“What's become apparent over recent years is that one inflammasome in particular – the NLRP3 inflammasome – is very important in a number of major diseases such as obesity and atherosclerosis, but also in diseases like Alzheimer's and Parkinson's disease, many of the diseases of older age people, particularly in the Western world.”

Fasting can help reduce inflammation, but the reason why has not been clear. To help answer this question, a team led by Professor Bryant and colleagues at the ̽��ֱ�� of Cambridge and National Institute for Health in the USA studied blood samples from a group of 21 volunteers, who ate a 500kcal meal then fasted for 24 hours before consuming a second 500kcal meal.

̽��ֱ��team found that restricting calorie intake increased levels of a lipid known as arachidonic acid. Lipids are molecules that play important roles in our bodies, such as storing energy and transmitting information between cells. As soon as individuals ate a meal again, levels of arachidonic acid dropped.

When the researchers studied arachidonic acid’s effect in immune cells cultured in the lab, they found that it turns down the activity of the NLRP3 inflammasome. This surprised the team as arachidonic acid was previously thought to be linked with increased levels of inflammation, not decreased.

Professor Bryant, a Fellow of Queens’ College, Cambridge, added: “This provides a potential explanation for how changing our diet – in particular by fasting – protects us from inflammation, especially the damaging form that underpins many diseases related to a Western high calorie diet.

“It’s too early to say whether fasting protects against diseases like Alzheimer's and Parkinson's disease as the effects of arachidonic acid are only short-lived, but our work adds to a growing amount of scientific literature that points to the health benefits of calorie restriction. It suggests that regular fasting over a long period could help reduce the chronic inflammation we associate with these conditions. It's certainly an attractive idea.”

̽��ֱ��findings also hint at one mechanism whereby a high calorie diet might increase the risk of these diseases. Studies have shown that some patients that have a high fat diet have increased levels of inflammasome activity.

“There could be a yin and yang effect going on here, whereby too much of the wrong thing is increasing your inflammasome activity and too little is decreasing it,” said Professor Bryant. “Arachidonic acid could be one way in which this is happening.”

̽��ֱ��researchers say the discovery may also offer clues to an unexpected way in which so-called non-steroidal anti-inflammatory drugs such as aspirin work. Normally, arachidonic acid is rapidly broken down in the body, but aspirin stops this process, which can lead to an increase in levels of arachidonic acid, which in turn reduce inflammasome activity and hence inflammation.

Professor Bryant said: “It’s important to stress that aspirin should not be taken to reduce risk of long terms diseases without medical guidance as it can have side-effects such as stomach bleeds if taken over a long period.”

̽��ֱ��research was funded by Wellcome, the Medical Research Council and the US National Heart, Lung, and Blood Institute Division of Intramural Research.

Reference
Pereira, M & Liang, J et al. Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting. Cell Reports; 23 Jan 2024; DOI: 10.1016/j.celrep.2024.113700

Cambridge scientists may have discovered a new way in which fasting helps reduce inflammation – a potentially damaging side-effect of the body’s immune system that underlies a number of chronic diseases.

Our work adds to a growing amount of scientific literature that points to the health benefits of calorie restriction

Clare Bryant

Carol Yepes (Getty Images)

Intermittent fasting conceptual image

Yes

Drug incorporated into silicone coating reduces ‘foreign body reaction’ to implants

cjb250 — Mon, 14 Mar 2022 20:00:59 +0000

Implantable electronic medical devices are already widely used for a number of applications, but they also offer the prospect of transforming the treatment of intractable conditions, such as the use of neural electrical stimulators for spinal injury patients.

There is one major problem, however: our body recognises, attacks and surrounds these implants with a dense, ‘protective’ capsule of scar tissue that prevents electrical stimulation reaching the nervous system.

This so-called ‘foreign body reaction’ is driven by an inflammatory response against the implant. First, immune cells known as macrophages attack and try to destroy the device. Then a more long-term response kicks in, again coordinated by the macrophages, which leads to the build-up of a collagen-rich capsule to separate it from the surrounding tissue. This response then persists until the implant is removed from the body.

̽��ֱ��mechanisms by which foreign body reaction occurs are poorly understood, meaning that there are no effective methods to prevent it without interfering with the tissue repair mechanisms, for example after nerve damage.

First author Dr Damiano Barone from the Department of Clinical Neurosciences at the ̽��ֱ�� of Cambridge said: “Foreign body reaction is currently an unavoidable complication of implantation and is one of the leading causes of implant failure. At the moment, the only way we have of preventing it is to use broad-spectrum anti-inflammatory drugs such as dexamethasone. But these are problematic – they may stop the scarring, but they also stop the repair.”

In a study published today in the Proceedings of the National Academy of Sciences (PNAS), scientists implanted an electrical device into mice to compensate for sciatic nerve damage and compared the response within the surrounding tissue to that in mice who did not receive an implant. As well as using normal mice, the researchers used mice whose genes controlling the inflammatory response had been ‘knocked out’, preventing a response.

This allowed the team to see how the body’s inflammatory response generated the foreign body reaction, and which genes were involved. In turn, this showed that a particular molecule known as NLRP3 plays a key role.

̽��ֱ��researchers then added a small molecule known as MCC950 to the device coating and tested its effect in the mice. MCC950 has previously been shown to inhibit the activity of NLRP3. They found that this prevented the foreign body reaction without affecting tissue regeneration. This contrasted with dexamethasone treatment, which prevents the foreign body reaction but also blocks nerve regeneration.

NLRP3 inhibitors are being developed for a number of clinical applications including inflammatory disease, cancer, sepsis, Alzheimer’s disease and Parkinson’s disease. They are already being tested in clinical trials for certain conditions.

Joint senior author Professor Clare Bryant from the Department of Medicine at the ̽��ֱ�� of Cambridge said: “There’s a lot of excitement around this new class of anti-inflammatory drugs. Once they’ve been through clinical trials and have been shown to be safe to use, we should be in a good position to integrate them into the next generation of implantable devices.

“Combining these drugs with different materials and softer coatings for devices could transform the lives of individuals who need long-term implants to overcome serious disability or illness. In particular, this could make a huge difference to neuroprosthetics – prosthetics that connect to the nervous system – where the technology exists, but scarring has not yet made their widespread use viable.”

̽��ֱ��research was supported by the Medical Research Council and Wellcome.

Reference
Barone, DG et al. Prevention of the foreign body response to implantable medical devices by inflammasome inhibition. PNAS; 14 March 2022; DOI: 10.1073/pnas.2115857119

Long-term use of implantable electronic medical devices – such as pacemakers and cochlear implants – is hampered by the body’s reaction to foreign bodies. Now, in a study in mice, a team led by scientists at the ̽��ֱ�� of Cambridge has shown that this reaction can be dramatically reduced by incorporating an anti-inflammatory drug into the silicone coating around the implant.

Combining these drugs with different materials and softer coatings for devices could transform the lives of individuals who need long-term implants to overcome serious disability or illness

Clare Bryant

Charles O'Rear (Getty Images)

X-Ray Showing Pacemaker

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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Farmed carnivores may become ‘disease reservoirs’ posing human health risk

jg533 — Tue, 24 Aug 2021 15:03:06 +0000

Farming large numbers of carnivores, like mink, could allow the formation of undetected ‘disease reservoirs’, in which a pathogen could spread to many animals and mutate to become a risk to human health.

Research led by the ̽��ֱ�� of Cambridge has discovered that carnivores have a defective immune system, which makes them likely to be asymptomatic carriers of disease-causing pathogens.

Three key genes in carnivores that are critical for gut health were found to have lost their function. If these genes were working, they would produce protein complexes called inflammasomes to activate inflammatory responses and fight off pathogens. ̽��ֱ��study is published today in the journal Cell Reports.

̽��ֱ��researchers say that the carnivorous diet, which is high in protein, is thought to have antimicrobial properties that could compensate for the loss of these immune pathways in carnivores – any gut infection is expelled by the production of diarrhoea. But the immune deficiency means that other pathogens can reside undetected elsewhere in these animals.

“We’ve found that a whole cohort of inflammatory genes is missing in carnivores - we didn’t expect this at all,” said Professor Clare Bryant in the ̽��ֱ�� of Cambridge’s Department of Veterinary Medicine, senior author of the paper.

She added: “We think that the lack of these functioning genes contributes to the ability of pathogens to hide undetected in carnivores, to potentially mutate and be transmitted becoming a human health risk.”

Zoonotic pathogens are those that live in animal hosts before jumping to infect humans. ̽��ֱ��COVID-19 pandemic, thought to originate in a wild animal, has shown the enormous damage that can be wrought by a novel human disease. Carnivores include mink, dogs, and cats, and are the biggest carriers of zoonotic pathogens.

Three genes appear to be in the process of being lost entirely in carnivores: the DNA is still present but it is not expressed, meaning they have become ‘pseudogenes’ and are not functioning. A third gene important for gut health has developed a unique mutation, causing two proteins called caspases to be fused together to change their function so they can no longer respond to some pathogens in the animal’s body.

“When you have a large population of farmed carnivorous animals, like mink, they can harbour a pathogen - like SARS-CoV-2 and others - and it can mutate because the immune system of the mink isn’t being activated. This could potentially spread into humans,” said Bryant.

̽��ֱ��researchers say that the results are not a reason to be concerned about COVID-19 being spread by dogs and cats. There is no evidence that these domestic pets carry or transmit COVID-19. It is when large numbers of carnivores are kept together in close proximity that a large reservoir of the pathogen can build up amongst them, and potentially mutate.

This research was funded by Wellcome.

Reference
Digby, Z. et al: ‘Evolutionary loss of inflammasomes in the Carnivora and implications for the carriage of zoonotic infections.’ Cell Reports, August 2021. DOI: 10.1016/j.celrep.2021.109614

Carnivorous animals lack key genes needed to detect and respond to infection by pathogens, a study has found.

We’ve found that a whole cohort of inflammatory genes is missing in carnivores

Clare Bryant

Oikeutta elaimille on Flickr

Farmed mink

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When Symptoms Don't Stop

jg533 — Fri, 22 Jan 2021 08:13:29 +0000

Treating those most severely affected by COVID-19 has necessarily taken priority during the pandemic. But could long COVID be the next wave of the crisis?

Cambridge Science Festival returns for milestone 25th year

Anonymous — Fri, 25 Jan 2019 15:48:27 +0000

Celebrating its 25th year, the Festival runs for two weeks from 11-24 March and explores the theme of ‘discoveries’. An impressive line-up of acclaimed scientists includes microscopist Professor Dame Pratibha Gai, Astronomer Royal Professor Lord Martin Rees, 2018 Nobel prize winner Sir Gregory Winter, geneticist Dr Giles Yeo, statistician Professor David Spiegelhalter, engineer Dr Hugh Hunt, marine biologist and author Helen Scales, THIS Institute Director Professor Mary Dixon-Woods, futurist Mark Stevenson, and science presenter Steve Mould.

̽��ֱ��full programme is teeming with events ranging from debates, talks, exhibitions, workshops and interactive activities to films, comedy and performances, held in lecture theatres, museums, cafes and galleries around Cambridge. There are events for all ages and most are free.
With so many events on offer, audiences will be spoilt for choice. Some of the biggest events in week one include:

Is technology making us miserable? (11 March). Virtually every interaction we have is mediated through technology. Despite being ‘always-on’, are we any better off? Are we better connected? Or is technology making us miserable?
Putting radioactivity in perspective (12 March). Following a renewal of electricity generated by nuclear power, Professors Ian Farnan and Gerry Thomas, Imperial College London, discuss radioactivity in the natural world and the outcomes of decades of study on the health effects of radiation. Could these research outcomes reset attitudes towards radiation and the risks?
̽��ֱ��universe of black holes (13 March). Christopher Reynolds, Plumian Professor of Astronomy, describes how future research into black holes may yet again change our view of reality.
̽��ֱ��long-term perspective of climate change (14 March). Professors Ulf Büntgen, Mike Hulme, Christine Lane, Hans W Linderholm, Clive Oppenheimer, Baskar Vira, and Paul J Krusic discuss how we investigate past climate and the challenges we face in applying this to the policy-making process.
Catalytic activation of renewable resources to make polymers and fuels (15 March). Professor Charlotte Williams, ̽��ֱ�� of Oxford, discusses the development of catalysts able to transform carbon dioxide into methanol, a process which may deliver more sustainable liquid transport fuels in the future.
Does the mother ever reject the fetus? (15 March). Professor Ashley Moffett discusses fetal rejection and explores new discoveries that show that there are multiple mechanisms to ensure there is a peaceful environment in the uterus, where the placenta is allowed to grow and develop to support the fetus.

Top picks for the second week include:

Cambridge gravity lecture: Sir Gregory Winter (18 March). Sir Gregory is a molecular biologist and 2018 Nobel Laureate best known for his work on developing technologies to make therapeutic monoclonal antibodies. His research has led to antibody therapies for cancer, rheumatoid arthritis and multiple sclerosis.
Discoveries leading to new treatments for dementia (18 March). Professor of Clinical Neurosciences and Associate Director of the UK Dementia Research Institute, Giovanna Mallucci discusses how new research leading to insights into dementia and degenerative brain diseases may lead to new treatments.
Improving quality and safety in healthcare (19 March). THIS Institute Director Professor Mary Dixon-Woods looks at the challenges to improving quality and safety in healthcare and considers why it’s so hard to answer the question: Does quality improvement actually improve quality? With Dr Fiona Godlee, Editor in Chief of ̽��ֱ��BMJ.
Immunology: the future of medicine? (19 March) Professor Clare Bryant and a panel of Cambridge immunologists discuss how understanding disease triggers may enable entirely new approaches to treating and potentially preventing disease.
Polar ocean: the dead end of plastic debris (19 March). An estimated 80% of all the litter in our oceans is plastic, and a significant concentration of plastics debris is found in both polar oceans. ̽��ֱ��impact of this debris on the sensitive polar ecosystem could be profound. Pelagic marine ecologist Dr Clara Manno, British Antarctic Survey, explores the current research and existing situation in the polar regions.
Reluctant futurist (19 March). Old models for healthcare, education, food production, energy supply and government are creaking under the weight of modern challenges. Futurist Mark Stevenson looks at the next 30 years and asks, how can we re-invent ourselves for the future?
Adolescent mental health: resilience after childhood adversity (20 March). Adolescence is characterised by huge physiological changes as well as a rapid rise in mental health disorders. Around 45% of adolescent mental health problems are caused by childhood difficulties but fortunately not all who experience difficulties develop mental health disorders. Dr Anne-Laura van Harmelen discusses mechanisms that may help adolescents with a history of childhood difficulty to become more resilient.
Making algorithms trustworthy (21 March). Increasingly, algorithms are being used to make judgements about sensitive parts of our lives. How do we check how their conclusions were arrived at, and if they are valid and fair? Professor David Spiegelhalter looks at efforts to make algorithms transparent and trustworthy, using systems that make predictions for people with cancer as an example.
On the future: prospects for humanity (22 March). Professor Lord Martin Rees argues that humanity’s prospects on Earth and in space depend on our taking a different approach to planning for tomorrow.

This year’s Cambridge Science Festival also celebrates significant milestones in science, including the 200th anniversary of Cambridge Philosophical Society, Cambridge’s oldest scientific society, and 150 years since the publication of the modern Periodic Table.

Speaking ahead of the Festival, Dr Lucinda Spokes, Festival Manager, said: “We are tremendously proud of this year’s programme due to the variety of events and the calibre of our speakers from a range of institutions and industries.

“Alongside the meatier topics we have an array of events for all ages and interests across both weekends. We have everything from the science of perfumery and how your mood affects your taste, to a science version of 'Would I Lie to You?'

“One of my personal top picks are the open days at the various institutes and departments based at the West Cambridge site on Saturday 23 March. As always, the site is hosting some truly fascinating events, everything from the future of construction and how to make Alexa smarter, to how nanotechnology is opening up new routes in healthcare, and state-of-the-art approaches to low-cost solar energy and high-efficiency lighting solutions.

“A Festival of this magnitude would not be possible without the help from many people; we thank all our scientists, supporters, partners and sponsors, without whom the Festival would not happen. Most of all, we thank the audiences – there are more than 60,000 visits to the Festival events every year. We very much look forward to welcoming everyone from all ages to join us in March to explore the fabulous world of science.”

You can download the full programme here.

Bookings open on Monday 11 February at 11am.

This year’s Festival sponsors and partners are Cambridge ̽��ֱ�� Press, AstraZeneca, MedImmune, Illumina, TTP Group, Science AAAS, Anglia Ruskin ̽��ֱ��, Astex Pharmaceuticals, Cambridge Science Centre, Cambridge Junction, IET, Hills Road 6th Form College, British Science Week, Cambridge ̽��ֱ�� Health Partners, Cambridge Academy for Science and Technology, and Walters Kundert Charitable Trust. Media Partners: BBC Radio Cambridgeshire and Cambridge Independent.

̽��ֱ��2019 Cambridge Science Festival is set to host more than 350 events as it explores a range of issues that affect today’s world, from challenges around climate change policy, improving safety and quality in healthcare, and adolescent mental health, to looking at what the next 25 years holds for us and whether quantum computers can change the world.

We have everything from the science of perfumery and how your mood affects your taste, to a science version of 'Would I Lie to You?'

Dr Lucinda Spokes

Yes

New innovation hub aims to take a 'moon shot' at cystic fibrosis

cjb250 — Wed, 18 Apr 2018 14:01:05 +0000

John Winn’s office at Microsoft Research looks like that of any typical academic: on one wall is a whiteboard graffitied with impenetrable equations and mathematical scribblings, on the opposite wall books and files line shelves, and on his desk are photos of his family.

His desk, however, is somewhat different: it can rise or fall, depending on whether he wants to work standing or sitting – and underneath is a treadmill for walking and working at the same time. “There have been times when I’ve been deep in thought and almost fallen off it,” he jokes.

Winn has cystic fibrosis (CF) and keeping fit is an important part of managing his condition: the stronger his lung function, the better equipped he is to fight the potentially life-threatening infections that plague people living with the condition.

CF occurs when an individual inherits two copies of a single genetic variant, one from each parent. ̽��ֱ��disease causes a build-up of thick, sticky mucous in the lungs, intestines and organs, and those affected by the condition are particularly susceptible to lung infections leading to progressive inflammatory lung damage. Although life expectancy for people with CF has almost doubled in recent decades, it is still significantly below average.

Winn is a machine learning specialist and is using his expertise to fight the condition that affects his everyday life. Together with Professor Andres Floto from the Department of Medicine at Cambridge, he is turning data from the daily lives of people with cystic fibrosis into potentially life-saving information.

As part of this study, funded by the Cystic Fibrosis Trust and Royal Papworth Hospital, participants have been submitting data – everything from heart rate and lung function through to self-reported wellbeing – via an app that also monitors their activity levels. Machine learning then sifts through the data, looking for patterns and – it’s hoped – building a model that can predict when a patient’s health is about to deteriorate and advise them to seek medical help.

“ ̽��ֱ��overarching principle is about giving people control over their own health data and making it work for them,” says Winn. “There’s some informal feedback that just participating in the study and taking these readings has already improved health outcomes for some individuals: for example, it’s helped with adherence with taking their medications as they noticed that if they missed taking certain medicines, their readings got worse.”

̽��ֱ��project is just one strand of a major new Cystic Fibrosis Innovation Hub based on the Cambridge Biomedical Campus and run by Floto. ̽��ֱ��Hub is supported through a £5 million commitment from the Cystic Fibrosis Trust and matching funds from the ̽��ֱ�� of Cambridge. It will strengthen existing collaborations across the ̽��ֱ�� and with the Wellcome Trust Sanger Institute, as well as build new collaborative research networks with CF centres around the UK. ̽��ֱ��Trust’s Chief Executive, David Ramsden, said it will “provide in CF research across the country”.

Floto agrees with this sentiment: “We have an opportunity to uplift UK CF research in general by providing knowhow, training and reagents in a number of areas including genomics, bioinformatics, stem cells and clinical trials technology.”

A major part of the Hub’s activities will be around developing new drugs that target chronic inflammation in CF, in collaboration with the pharmaceutical company GSK as part of the GSK/Cambridge Strategic Partnership, as well as new antibiotic therapy for the main causes of lung infection in the condition.

Finding new drugs against these bacteria is becoming increasingly urgent – Floto and Professor Julian Parkhill at Sanger recently showed that Mycobacterium abscessus, the pathogen behind one of the most serious infections, is becoming increasingly multi-drug resistant and spreading globally. This is one reason why people with CF are advised not to meet each other.

“Clearly the techniques that we develop – and the drug-like molecules that come out of it – will have more general applicability to patients with other multi-drug resistant infections,” Floto says. This will be welcome news to England’s Chief Medical Officer, Professor Dame Sally Davies, who has warned of a future where “any one of us could go into hospital in 20 years for minor surgery and die because of an ordinary infection that can’t be treated by antibiotics.”

̽��ֱ��timing of all this is particularly good: Papworth Hospital, whose Adult Cystic Fibrosis Centre has gained a national and international reputation for its treatment of patients and its contribution to research, is due to move to the Biomedical Campus later in 2018. ̽��ֱ��CF wards will feature state-of-the-art air flow systems, designed with Floto’s work on the spread of multi-drug resistant CF pathogens in mind.

This close proximity between the patients and the researchers will help Floto test the new treatments he is pioneering. He is particularly excited about the potential for new cellular therapies he’s developing with Professor Ludovic Vallier at the Department of Surgery. Floto describes these as their “moon shot”. These would involve taking cells from a CF patient, re-programming them – correcting the genetic defect along the way – and then re-injecting them into patients. “This could provide a way to regenerate damaged lungs,” he says.

Floto knows his plans for the Hub are ambitious, but given that it’s almost 30 years since the gene that causes CF was discovered and there is still no cure for the disease, believes it’s time to take this shot at the moon.

Floto’s collaborators in the CF Innovation Hub include Chris Abell (Chemistry), Sir Tom Blundell (Biochemistry), Julian Parkhill and Ludovic Vallier.

Almost 30 years on from the discovery of the genetic defect that causes cystic fibrosis, treatment options are still limited and growing antibiotic resistance presents a grave threat. Now, a team of researchers from across Cambridge, in a major new centre supported by the Cystic Fibrosis Trust, hopes to turn fortunes around.

We have an opportunity to uplift UK cystic fibrosis research in general by providing knowhow, training and reagents in a number of areas including genomics, bioinformatics, stem cells and clinical trials technology

Andres Floto

Cambridge Biomedical Campus

A no-strings-attached scientific relationship

Professor Claire Bryant, like Floto, works on an inflammatory lung disease as part of the GSK/Cambridge Strategic Partnership. In her case, she’s looking at chronic obstructive pulmonary disease (COPD).

COPD is a condition caused by smoking, pollution and severe asthma. Bryant is looking in particular at how COPD makes the lungs ‘stickier’ to bacteria, increasing the risk of infections.

She holds two grants under the GSK/Cambridge Strategic Partnership, which aims to develop the next wave of ‘game-changing’ medicines by bringing academic and industrial expertise together to tackle often intractable disease. Based at Cambridge’s Department of Veterinary Medicine, Bryant currently has a three-day-a-week sabbatical at GSK’s headquarters in Stevenage. As such, it’s arguable whether anyone embodies the partnership more than she does.

̽��ֱ��three-year sabbatical provides Bryant with three postdocs, two PhD students and budget, with access to GSK resources, but with “no strings attached”. ̽��ֱ��only proviso is that if she works with a GSK reagent, they have first rights on what she does with this. Crucially, she says, it gives her “the space to think”.

Bryant is embedded in GSK’s Respiratory Drug Discovery Unit and attends its lab meeting every week. “I’ve met really smart, clever scientists at GSK, with different skills to those of us in academia,” she says. “I get to see all aspects of what happens at GSK, everything from how a target is identified to how drugs are developed to target it, through to taking these drugs to clinical trials. I see the whole spectrum.”

It is, though, a mutually beneficial programme, she stresses. Bryant brings her knowledge of innate immunity and her experience of multi-disciplinary collaborations, particularly in imaging. “It’s effectively like being a consultant,” she says. “I want them to get as much out of me as I do out of them.”

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