Uncategorized

Building polymicrobial biofilm models with Brogan Richards, a PhD candidate based at The University of Nottingham. This research is focused on developing polymicrobial pre-clinical models of CF lung infections. Brogan is working closely with Dr Jo Fothergill on PIPE-CF, an SRC co-funded by the Cystic Fibrosis Trust and Cystic Fibrosis Foundation. We caught up with Brogan to find out more about his research.

Can you tell us a little about the focus of your research? What are the challenges are you trying to address?

My project is about generating a polymicrobial biofilm model that resembles those seen in the CF lung. This in combination with the other PIPE-CF PhD students will create a more specific group of pre-clinical models that will hopefully increase the number of antimicrobials reaching the clinical testing stage.

What might the implications of your research be on the management of infections in people with CF?

My research would hopefully result in increased control of CF infections as well as reducing the number of CF patients taking ineffective antibiotics. This research would also hopefully increase the chances of new and improved antimicrobials making it into the clinics.

How important is collaboration in your work? Are there any areas of research in particular that you’re looking to collaborate in?

Collaboration plays a major role in my role. My PhD is half of a project in collaboration with Hollie Leighton looking at developing a polymicrobial biofilm model and our joint project is just one piece of the puzzle in collaboration with PIPE-CF PhD students and labs across the world. All these pieces together will hopeful improve and increase standardisation of the whole pre-clinical pipeline for testing existing and novel antimicrobials related to CF. I love being involved in cutting edge research and if I could help someone or they could help me then I would love to collaborate.

How did you get into CF antimicrobial research, and why do you find it so interesting?

I have always had a passion for bacteriology and antimicrobial resistance and the way bacteria always seem to have the advantage. In regard to CF, there is so much research being carried out and yet so much more is needed to ensure that CF patients get the best care and best outcomes.  I especially have an interest in developing new models of CF which currently does not reflect the same level of advancements as other areas of CF research.  CF also adds an extra layer of complexity in the field of AMR which results in a high rate of antibiotic failure and a lack of standardisation in the antimicrobial pipeline which I feel passionate about improving.

Research wise, what are your next steps?

The next big step in my project is to hopefully add additional complexity to my model and increase the utility and clinical relevance. Hopefully alongside this I can look into what makes my bacteria tick.  I am always looking for new and interesting ideas in this field and so if anyone wants to talk science please get in touch.

We caught up with Tom Barton, whose PhD is focused on developing laboratory models testing novel antimicrobial treatments in Cystic Fibrosis. Tom is working closely with Dr Jo Fothergill on PIPE-CF, an SRC co-funded by the Cystic Fibrosis Trust and Cystic Fibrosis Foundation. His paper,  ‘Challenges and opportunities in the development of novel antimicrobial therapeutics for CF’ was recently published in the journal of medical microbiology.

 Tom, can you tell us a little about the focus of your research?  

My PhD focusses broadly on developing models of cystic fibrosis infection that can be used to test new antimicrobial treatments, so that we can more efficiently develop effective treatments for infection. Specifically, I focus on models that involve the host response, those that include not only pathogens, but factors involved in the human response to CF infection. An example of this includes incorporating, host cells and immune components in our models. We hope to optimise models that can accurately predict success of potential antimicrobial treatments, so that individuals with cystic fibrosis get more effective antimicrobials, faster.   

In your paper, you identify collaboration within the CF community as an opportunity to be seized when it comes to antimicrobial drug discovery. Can you tell us why you think this is so important? 

For CF antimicrobial research to be effective in improving the lives of people with CF, researchers must collaborate with those affected to identify priorities in future research. While eradication of infection is of primary concern, reducing unwanted side effects and lowering the burden of antibiotic regimens is also important – conclusions that can only be arrived at through collaboration with the CF community. To be effective in our response to CF infection, we must communicate with people with CF to ensure we remain focussed on maximally benefitting each aspect of their life.    

You attended the cross collaborative PIPE-CF and  UKCFIB joint workshop last year- what did you enjoy most about the workshop? 

The workshop provided a forum for researchers, industry, policymakers and others to share views and ideas, which provided a unique perspective on CF research. This is invaluable, as it contextualises the research being carried out and gives clarity to the direction CF research will take. I think this is the most impactful part of the workshop.   

What were your key take-aways from this event?  

My key takeaways from the meeting include the opportunity to develop novel antimicrobial treatments for CF infection, and the focus on developing robust, representative models to improve the efficiency of developing new drugs. Novel antimicrobials, such as anti-virulence treatments that reduce the severity of infection could be instrumental in improving infection outcomes. Meanwhile, there is considerable opportunity for researchers to develop models that accurately mimic key aspects of the CF lung environment. Optimisation of our CF models will accelerate antimicrobial development, which I hope will lead to considerable improvements in infection outcomes in the future.  

Are there any areas of research that you’re looking to collaborate in? 

We have a strong focus on incorporating the host CF environment into our models, to gain more accurate insight into how potential antimicrobial treatments perform before they enter clinical trials. Any collaboration associated with host-pathogen models would be ideal.  

How did you get into CF antimicrobial research, and why do you find it so interesting? 

Cystic fibrosis arises through a relatively simple mechanism, giving rise to a multifaceted problem with significant impacts on the lives of those with the disease. Understanding CF infection requires an understanding of how the host environment is altered and how bacteria and other pathogens live and communicate in the lungs. My PhD project is immensely interesting to me as it allows me to learn how these factors interact, and how we may model the environment to facilitate the development of CF antimicrobials. I hope the work we are doing may have a strong impact on CF antimicrobial development, and therefore on the wider CF community.  

Addressing cystic fibrosis challenges together: Takeaways from a cross-sector workshop. Hollie Leighton is doing her PhD at the University of Liverpool and is part of a group of academics working on PIPE-CF led by prof Jo Fothergill. Her research focuses on developing a liquid polymicrobial biofilm model for use in the pre-clinical pipeline to develop new cystic fibrosis antimicrobials.

Hollie attended a PIPE-CF/ UKCFIB joint workshop held in October 2022. The workshop was designed to stimulate thinking around focus areas of innovation needed to optimise the tools and resources available for preclinical Cystic Fibrosis antimicrobial medicines discovery.  We caught up with Hollie to learn more.

How did you learn about the workshop and what prompted you to sign up?

I learnt about the workshop through my supervisors as my PhD is part of PIPE-CF along with three other PhD students. I was excited to have the opportunity to meet with other researchers in the field, along with clinicians and CF patients, and learn how my research would contribute to having an impact on the wider community.

What did you enjoy most about the workshop?

I really enjoyed learning about other research that is taking place within the field, such as the organ-on-a-chip technology that was presented, which aims to model human organs and can reproduce CF-like conditions. It can also represent niche environments such as the sinuses and the lungs which aren’t currently differentiated between in most models used in the drug development pipeline.

What was your key takeaway from the event?

The biggest takeaway from the event from me was the general feeling among attendees that there is a disconnect between researchers and clinicians, and people with CF. Factors such as administration routes, side effects and time needed in clinics are not always considered by researchers when new therapeutics are being developed, when it is important that treatments fit into the busy lifestyles of people with CF. It is important that researchers connect with the CF community frequently to ensure that quality of life for the patients can be maintained while effective treatments are delivered.

What key insights would you share with other researchers working in CF AMR?

One of the challenges facing researchers at the moment is determining biomarkers for positive clinical outcomes of antibiotics, as the success of a new drug in clinical trials is primarily based on improving quality of life, which does not always translate to numerical data in the lab.

Also, the chronic aspect of the disease is frequently overlooked in model development as well, so the long-term consequences are not considered when determining the success of a therapeutic. Many models focus on a 24-hour growth time of the pathogen in a planktonic state, meaning the chronic nature of biofilms is ignored.

Is there anything else you would like to share about your experience?

Current in vitro models that are used in the drug development pipeline are not representative of the environment that infections occur, with biofilm formation and polymicrobial communities being frequently overlooked. This makes it difficult to predict how the drug will perform in the clinic. While new technologies such as the organ-on-a-chip system are being developed, the presentations delivered at this event emphasise the need for continued research within these areas.

What other workshops would you like to see the CF AMR Syndicate run?

I would really like to learn more about how the antimicrobial resistance problem is being faced by drug developers and clinicians, and how awareness is being spread to other members of the community. AMR is an ever increasing problem, especially among people living with CF, and it’s important that research is continued and shared to be able to deal with it.

Read Abi’s story of how having Cystic Fibrosis and living with a chronic infection has affected her life. Abi is an active contributor to the CF AMR Syndicate’s steering committee.

I’m Abi. I’m a 31-year-old cystic fibrosis (CF) patient with a chronic burkholderia infection.

As a child, my CF was almost atypical. I was pancreatic insufficient and had a slightly unhappy liver, but other than I was “normal”. My FEV1 was in the late 90s and occasionally early 100s, and I did everything my non-CF friends did. Yes, I took regular creon, vitamins, ursodeoxycholic acid, supplements and a prophylactic antibiotic, but I never had any issue with my chest or bowels. I exercised well, kept away from the hospital for everything but quarterly clinic appointments, and my twice-daily physio never produced even a fleck of mucus. I was healthy to a level where my CF didn’t feel real, and I would explain it whilst taking my meds to friends as “horrible for most, but luckily, I only have it mildly.”

When I’d just turned 16 my luck seemed to run out overnight when my paediatric consultant called to say my recent cough swab had cultured a rare burkholderia. He didn’t have much to say, and as my health hadn’t changed he decided to adopt a “watch and wait” approach whilst repeating the swab. 2 weeks later at clinic he confirmed that this had also cultured the same bug, which had been identified as burkholderia gladioli. I couldn’t start any antibiotics for it as it was still being tested for its exact weaknesses.

By 16, I already had a good understanding of CF and the nastier bugs. Pseudomonas had felt like an ever-present danger that I’d somehow miraculously swerved and as a 90s child my bigger fear was cepacia. Catching a burkholderia that wasn’t cepacia was a complete curve ball. The lack of information about both what it would do and how to treat it was deeply distressing. My doctor had no information he was willing to provide me with, instead telling me not to worry; the gladioli would likely just sit dormant in my lungs till he could eradicate it.

Despite my fears, my doctor was right. The gladioli didn’t suddenly wreak havoc in my lungs, my lung function stayed high, I remained symptom free and carried on living normal life like I always had. My doctor decided it wasn’t the time to start eradication treatment as I was on the cusp of moving up to adults. Over the following 18 months, the gladioli grew on every single cough swab, and at my first adult unit appointment, I was informed that eradication was now not worth pursuing. As my health was still good no additional antibiotics were added into my regime on the basis that burkholderia gladioli is vulnerable to so few they shouldn’t be wasted.

At the age of 21 I moved my CF centre. Although I was still very healthy within a year of the move, I had become unwell enough that I needed my first-ever IVs. This was a hard experience as I was very sick from the combination of meds, a common feature of the brutal regimes used for burkholderia. I had lost weight from the exacerbation and lost even more from the IVs. At the time, I thought it was tough, but now I’m 9 years into increasingly frequent IVs, I can see the first time was a walk in the park compared to IVs nowadays. The combinations make me horrendously sick unless IV anti-sickness is administered with every dose; I get brain fog, terrible diarrhoea, rashes, itching, painful pins and needles, temperatures, elevated liver levels and recently a heart rate of 151 just lying in bed.

Although the side effects of the IVs are hard to handle, the ever-increasing number of courses is the more alarming factor. When I have an exacerbation, I usually experience fevers, shortness of breath, joint pain, strong pain in both lungs and sometimes full night sweats. My Fev1 has never been too badly affected (baseline still in the 60s), but the symptoms of exacerbations are becoming worryingly regular. Last year I had 5 IV courses and a 6-week course of additional orals, the year before 6 lots of IVs. Every exacerbation I start hopeful with orals then wind-up doing IVs anyway. Sadly, a decision was agreed recently that I should have my IVs as an inpatient due to my lowered ability to tolerate the meds. I’m sure you can imagine the stress regularly yet randomly taking 2 weeks out from work and family life (I have 3 children) causes, but my antibiotic allergy list is now laughably long and with options being limited, “allergic” doesn’t always mean “don’t prescribe”, it’s more “prescribe with caution”.

In between exacerbations, I nebulise meropenem and tobramycin alternate months to try and keep a lid on the infection. These nebs are my biggest frustration and the worst part of my daily CF treatment burden. Meropenem neb is an off-label use, so I must mix it up like I would for an IV and inhale it through an e-flow over 25 minutes twice a day. Tobramycin takes about 20-25 minutes twice a day, too, but is at least a premixed med in a small plastic vial, which saves prep time.

For me, the worst part of this unpleasant situation is the knowledge that there’s nothing coming to change it. The antibiotics burkholderia reacts to are all quite old now and there’s nothing in the pipeline. My increased treatment has simply been more of the same, not anything new. It often feels that it’s the forgotten bug. It only really affects CF patients, and thankfully cross infection policies have meant it’s no longer epidemic at centres. The only patients who have it are the few who have been somehow unlucky enough to pick it up randomly.

The advent of modulators has changed the landscape of Cystic Fibrosis for many, but it is still early days.

Although Kaftrio especially is wonderful for many we do not know its long-term efficacy. Unfortunately, not everyone is eligible for modulators and some of those eligible are unable to tolerate. I am sadly in the group of patients who have had to come off due to intolerable side effects. But even those doing well with modulators now will need new antimicrobials in the future. CF may seem different now, but it has not gone.

From my personal experience there is an undeniable gap in research for burkholderia despite its poor prognosis, leaving a bleak situation for CF patients. I very much hope that the CF AMR syndicate will help plug it, providing a brighter future for those suffering now and those unfortunate enough to catch it in the future.

We caught up with Dr Ajay Mistry, CEO, to discuss identifying new drug targets with Oppilotech. Oppilotech is an innovative UK SME that accurately simulates biological processes using its unique predictive computational modelling platform, which provides new insights into treating diseases.

Ajay, can you tell us about Oppilotech?

Oppilotech is developing a pipeline of first-in-class drugs. To do this, we have used systems biology and machine learning to build some of the most detailed computational models of bacteria ever assembled. Our proprietary computational methods accurately simulate and track biochemical processes in cells at unprecedented levels of resolution. This provides deep insights into biology, which traditional methods could not have identified before, enabling us to identify non-intuitive, viable targets for drug intervention. We then develop drugs against these targets. As a Company, we’re science-driven, passionate about the impact of our work on patients as well as being a fun place to work!

Why is it so important to select the right drug target, and how does your computation model help?

One of the most important challenges in drug discovery in any therapeutic area be it antibacterials, cancer, inflammation etc..  is identifying the most relevant biological target to aim the therapeutic efforts against. A selective high-quality drug molecule be it a small molecule, an antibody, RNAi or other modalities, will never become a medicine if it is modulating the wrong target. The unfathomable complexity of biology within cells often surprises scientists which can turn a promising drug target into a redundant one further down the development path. Often at a cost of millions of pounds and years of work. Even bacteria, are highly complex organized entities. An E.coli bacteria for example has around 4000 genes, which transcribes over 10 million different RNA species that can be translated into 132 million different proteins and producing over 300 million different metabolites. These components are highly organized, interactive moving parts all in a cell with a volume of 0.7micrometer cubed! Unravelling this complexity provides insight into optimal targets to inhibit –  and that’s what our computational models aim to do. Cross the complexity gap and identify connections that not even the greatest human experts can do, due to the limitations of the human mind.

Can you tell us about any of the drug discovery programmes you have ongoing? How are they relevant to cystic fibrosis?

We have several early-stage programmes based on targets identified using our bacterial models. The programmes are all targeted at the difficult to treat Gram-negative group of bacteria and if successful would represent novel antibiotic classes. One of our programmes (OPT200) targets the biosynthesis of Lipid A, a component found in the outer envelope of Gram-negative bacteria such as Pseudomonas aeruginosa, which I’m sure you know is frequently associated with CF infections. Recently we have entered into co-development partnerships on two novel targets with Evariste Technologies (based in the UK) and Peptris (based in India). The partners have developed ligand discovery platform technologies that significantly cut the time required to identify clinical drug candidates. With all our programmes, we ensure that during the screening process we include panel of CF relevant clinical isolates thereby selecting for compounds that work against these bacteria.

Oppilotech has also developed microbiology lab services. Can you tell us a bit more about your offering and how the CF AMR community can get access?

Our Director of Microbiology Ed Siegwart has worked in CRO microbiology screening business for over 12 years. When he moved to Oppilotech he was still getting requests for service work, so we decided to set up microbiology services business. Ed is very passionate about helping early-stage companies developing antibacterials. We are well aware of the fund raising and commercial challenges for companies developing antibacterials so we offer work in a flexible, collaborative capacity to help companies generate key data packages to reaching their milestones. We have an extensive bacterial isolate collection of over 25000 bacterial isolates including CF pathogens. We offer a range of lab-based services including MIC, MBC, Checkerboard assays, Time kill etc. In addition, we can also undertake simulation projects using our bacterial computational models. We have worked with start-ups straight out of University through to Big Pharma clients. They include companies developing antibacterial assets specifically for infections associated with CF. We are very approachable – so if any of the CF communities require isolates, help with screening or just want to know what we do –  come talk to us!

What’s next for Oppilotech?

We’re going to continue pushing the development of our internal programmes toward the clinic and expanding our services so we can work with more companies in the antibiotics space. In addition, we’re always open to partnerships around our modelling to see if there is scope to initiate additional drug discovery programmes.

Identifying new drug targets with Oppilotech, an interview with CEO Dr Ajay Mistry.

We caught up with Dr Sam Westgate, CEO of Perfectus Biomed Group. Perfectus are leaders in standard and customized microbiology testing services for a variety of sectors, including infectious disease. Recently, Perfectus has worked closely with Dr Freya Harrison at the University of Warwick on the Ex-vivo Porcine Lung Tissue Model. This model provides scientists with a test method that utilises a biological substrate to mimic human lung tissue especially useful in the study and treatment of chronic lung infection, including Cystic Fibrosis.

Sam, can you tell us a little more about Perfectus Biomed Group?

Perfectus Biomed was incorporated as a CRO that specialised in offering leading expertise in infection models that incorporate bacteria grown within a biofilm. Over the last decade our offering has expanded. We still specialise in the design and development of customised microbial methods, but this is now supported by microbiology, cell biology, virology and molecular biology.

What services do you offer that are relevant for cystic fibrosis antimicrobial research?

When companies are developing novel products, we support them throughout their development journey from formulation screening through to GLP testing for regulatory submissions. We offer a range of in vitro studies relevant to cystic fibrosis antimicrobial product development ranging from high throughput biofilm screening methods through to our accredited ex vivo epithelial lung tissue model.

Can you tell us a little more about your collaboration with Dr Freya Harrison, and the Ex-vivo Porcine Lung Tissue Model.

At Perfectus we have a proven track record of taking complex biofilm models and putting them through a rigorous validation process so as to fully understand and validate the methods and achieve UKAS accreditation. Dr Freya Harrison developed an excellent tissue model, appropriate for screening antimicrobial formulations against mucoid biofilms formed on ex vivo lung tissue. A joint collaboration allowed us to fully validate this method and gain independent UKAS accreditation to ISO 17025 standards. Ultimately this allowed us to offer a fully accredited ex vivo cystic fibrosis biofilm tissue model that can be used to de risk clinical studies and reduce in vivo testing.

How can the CF AMR community access your services?

Please feel free to contact us directly via info@perfectusbiomed.com, via our website or via phone on +44 1925 737 237. Our team of PhD scientists will be happy to discuss your project and microbiological models to suit your requirements.

What’s next for Perfectus Biomed Group and Cystic Fibrosis?

The role of biofilms within cystic fibrosis infections is becoming ever more recognised. There are many aspects of this ranging from the causative pathogen, understanding biofilm initiation and development and the treatment of persistent biofilm infections. Models that can mimic each of these stages and assess potential treatments are required in order to support the development of novel, effective treatments. It is critical that these models are proven to be applicable and reproducible. Our goal is to continue to develop appropriate methods and to use them to accelerate the research and development phase of novel Cystic Fibrosis biofilm treatments.  In short, we want to help in the development of effective treatments and products that reduce the symptoms of chronic infections.

Dr Rebecca (Beky) Weiser is a Postdoctoral Research Associate at Cardiff University, she is currently investigating the diversity and evolution of the lung microbiota in children with cystic fibrosis (CF). Beky works closely with Professor Esh Mahenthiralingam, who sits on the CF AMR Syndicate Steering Committee, and Dr Julian Forton. In this blog post, we caught up with Beky to find out more about her research.

Beky, can you tell us a little about your research; what are the challenges you’re trying to address?

 I am currently working as a researcher-co-investigator on a project funded by the US Cystic Fibrosis Foundation to investigate the lung microbiota in children with CF. This is challenging as children with CF often do not expectorate sputum even when unwell, meaning that other methods of sampling are needed to detect if they have microbial infections. Current routinely used sampling methods for children have limitations, as cough swabs are easy to perform but insensitive, and the gold standard sampling technique bronchoalveolar lavage (BAL) is invasive (it requires general anaesthetic) so cannot be performed frequently.

Working with the Cystic Fibrosis Sputum Induction Trial (CF-SpIT), we are evaluating the performance of induced sputum (IS) sampling for detecting specific antimicrobial resistant pathogens and the microbiota in the lower airways. As IS is non-invasive and can performed frequently, it can be used to collect multiple longitudinal samples. If IS can accurately capture the lung microbiota, we can use it to aid pathogen diagnosis, build up a picture of microbiota evolution and then start to understand the short- and long- term effects of antibiotic treatment on lung infections. This is really exciting as current sampling techniques for children with CF cannot be used in this way.

What results have you generated so far?

The previous culture microbiology work of CF-SpIT trial revealed that IS outperformed cough swab and matched the performance of the gold standard BAL in terms of pathogen detection. My project extends this work by using sensitive culture-independent (DNA based) techniques such as microbiota analysis to identify the different bacterial species in matched IS and BAL samples. So far, by looking at BAL samples we have found that microbiota compartmentalisation can occur in the lower airways of children with CF. This means that different bacterial communities are found in different lobes of the lung and presents problems for consistent microbiological sampling. We have also found that in approximately 80% of cases, IS captures a microbiota signature representative of one or more of the BAL samples taken from the lower airways, identifying the dominant or prevalent bacterial species. These results are promising, indicating that IS can reliably aid pathogen diagnosis and be used to understand microbiota evolution, even when lower airway samples may be variable.

How does your research relate to or impact on people with CF?

The CF-SpIT study has already had an impact on CF care, with many centres in the UK now performing IS routinely and other centres in Europe, the USA and Australia reconsidering their approaches to regular sampling in children. Using IS sampling and molecular diagnostics we will be able to improve pathogen detection and understand the impact of different treatments (including antibiotics) on the microbiota and disease progression. In addition, as many adults with CF who are taking CFTR modulator therapies are now expectorating less, IS may present a viable alternative to sputum samples to diagnose and monitor lung infections in adults.

Fig 1: The different microbiota profile types found by our study. ​ This figure shows the 8 different microbiota profile types found from the 30 sample sets in the study. Samples are grouped by sample set number and whether BAL samples are (a) concordant (similar), or (b) discordant (dissimilar). The performance of IS in relation to BAL samples is also noted. The top 25 most abundant genera/families across the sample set are indicated in the colour key. In 24/30 (80%) of cases, IS captured a microbiota signature representative of one or more of the BAL samples taken from the lower airways, identifying the dominant or prevalent bacterial species (profile types 1, 2, 3, 4, 6 and 7).

Full findings from Beky’s research have been published in the Journal of Cystic Fibrosis and can be accessed here

 What’s next for your research?

 As you may have expected from the above results, we are now analysing a large collection of IS samples, including longitudinal samples, to investigate microbiota evolution and correlate bacterial diversity to clinical parameters such as antibiotic treatments. At the same time, we are also using microbiota analysis to look at the fungal communities in CF-SpIT samples. This is really interesting and important as relatively little is known about the prevalence or clinical impact of fungi in CF, particularly in children.

 How did you get into CF antimicrobial research, and why do you find it so interesting?

 All of my research projects have had some link to CF research, whether it was researching antibiotic resistant bacterial species that are common pathogens in CF lung infections (Pseudomonas aeruginosa and Burkholderia cepacia complex species) or assisting clinical trials by performing microbiota analysis on CF samples. I have also worked with a company, AlgiPharma AS, who were carrying out a clinical trial on a new therapeutic, Oligo G, for these antibiotic resistant bacteria. I enjoy working with different collaborators and the translational aspect of the work I have done. It is great to think that something you are researching can positively impact the lives of people with CF.

I also find the data analysis process really interesting! I only really started learning bioinformatics and statistics for microbiota analysis during my first postdoctoral position. This was quite daunting as I hadn’t previously thought of myself as being particularly good at these things! Learning these skills has really opened my eyes to the world of data analysis, particularly to the tools and approaches used for analysing large datasets such as those used in microbiota research. I really enjoy exploring the data and working out the best approach to answer my research questions.

How important is collaboration in your work? Are there any areas of research/capabilities in particular that you’re looking to collaborate in?

 As this research is very translational, collaboration has been extremely important at every stage, from sample collection and processing to data analysis and results interpretation. We have regular meetings as a project team to ensure that we are asking the right questions in our analysis and that we can understand the clinical significance of the results. It has been a really useful experience to see how academic research can inform clinical practice.

As microbiota analysis is a complex and dynamic area of research, I hope that in the future I can collaborate with other bioinformaticians and statisticians to ensure that I am using the most up-to-date tools and models in my work. In particular, I would like to use microbiota analysis to look at co-occurrence of different species in CF lung infections and generate hypotheses about species interactions that can be tested in vitro in the lab.