PhD Projects 2026

The CDT is currently recruiting to the following PhD projects to start in September 2026. See below for details of each project, including the academic supervisors. Find out details of how to apply here.

Developing liver-on-a-chip platforms to assess beam radiation induced injury

Supervisors: Dr Neil Dufton, William Alazawi

Radiotherapy remains one of the most cost-effective cancer treatments worldwide. However, the liver represents both an unmet clinical challenge for primary and metastatic hepatic tumours and a critical organ at risk in many radiotherapy applications, including molecular radiotherapy using radiopharmaceuticals. The onset of radiation-induced liver disease (RILD) is a main limiting factor and it can take many months to develop and often go undetected until later stages of liver dysfunction. It is therefore essential to determine the impact of radiation exposure on the local and systemic microenvironment at early timepoints to develop new diagnostic and therapeutic strategies to mitigate the adverse effects. This project aims to tackle these challenges by developing in vitro models of RILD that can be used to assess the impact of radiation on individual and multicellular responses.

1. We will develop single cell cultures in an Ibidi flow system in series to assess and quantify radiation the effect of radiation on both directly exposed and shielded, but interconnected, samples.

2. We will investigate the response of beam-radiation therapy in a multicellular environment using Emulate liver-on-a-chip platforms. Cell responses to radiation will be assessed by combining live cell imaging with molecular biology techniques to measure transcription and proteomic changes in individual cells and their influence on released mediators.

To ensure physiological and clinical relevance, the model, particularly the Emulate platform, will be benchmarked against known liver radiation responses reported in clinical and preclinical studies. Together, this studentship will determine how complex in vitro models can be used to improve diagnostic tools and screen novel therapeutic targets to prevent RILD.

Developing an advanced glomerulus-on-a-chip model to study inflammation in the kidney

Supervisors: Dr Maria Fragiadaki, Prof Thomas Iskratsch

Details to follow, awaiting confirmation from Vertex Pharmaceuticals

3D printed chips to integrate cerebral organoids in electrode array systems and for neurotoxicity testing

Supervisors: Dr Isabel Palacios, Prof Julien Gautrot

Novel 3D brain models provide physiologically relevant platforms for assessing neurotoxic chemicals by closely replicating human brain architecture and development. Cerebral organoids in particular recapitulate neuroepithelial differentiation and early brain patterning. Multi-electrode arrays (MEAs) enable non-invasive, high-speed recording and stimulation of neuronal activity. However current organ-on-chip designs do not allow the integration of cerebral organoids with complex 3D MEAs. This project addresses this engineering gap by developing microfluidic platforms that embed 3D MEAs for the long-term culture, maturation and functional neurotoxicity tests of cerebral organoids.

Key objectives include:

1. Chip Engineering: We will design and fabricate microfluidic MEA-integrated chips using DLP 3D printing, commercial MEAs, and bespoke conductive polymer fibres (PEDOT, in collaboration with Chris Chapman). We propose a modular platform for the integration of complex 3D networks of electrodes, as well as commercial MEAs within the engineered microfluidic systems. Devices will be characterised by microscopy, profilometry, and conductivity/potentiometric testing, to validate fabrication fidelity and electroactive performance.

2. Organoid Integration and Interface Engineering: Cerebral organoids will be incorporated at selected development stages to assess how chip architecture, material interface biochemistry and electrode positioning impact on cell differentiation and long-term integration. Characterisation of critical markers associated with maturation of neuroepithelia and neuronal specification will be via immunostaining and confocal microscopy, qPCR, western blotting, proteomics, and RNAseq. MEA-based electroactivity profiles will be used to benchmark the engineered platform against conventional 2D systems.

3. MEA-Enabled Neurotoxicity Testing: A panel of five neurotoxic agents will be tested. Initial surrogates suitable for evaluation at QMUL will be used, followed by validation at DSTL facilities. Functional activity in response to these compounds will be evaluated via MEAs and correlated with possible changes in organoid structure and cellular composition (immunostaining and confocal microscopy).

Organ-on-a-chip model to probe key bottlenecks in tumour progression

Supervisors: Dr Adrian Biddle, John Marshall

Tumours progress through key bottlenecks; initiation, tissue invasion, intravasation, survival in circulation, extravasation, and growth at a metastatic site. Understanding the precise cellular changes driving tumour progression through these bottlenecks is important to enable the identification of new therapeutic targets for improved cancer therapy. However, the lack of suitable experimental models has hampered the detailed analysis of these cellular changes and their molecular underpinnings. In vivo models can recapitulate the breadth of these bottlenecks, but possess serious limitations; they are intractable to detailed investigation and extremely low throughput.

This project aims to develop an in vitro engineered model that can recapitulate key bottlenecks to tumour progression for detailed high-content analysis of dynamic processes. We will use the Kirkstall QV1200 system for its modular setup, continuous perfusion, and optical clarity. Using this system, we will address an engineering problem: how to merge static laboratory models with a system under continuous perfusion, whilst maximising ability to take detailed measurements. Models address different tumour bottlenecks:

1. An organotypic model of oral squamous cell carcinoma tumour initiation from normal oral mucosa.

2. A vascularised in vitro tumour microenvironment with fibroblast remodelling and immune cell infiltration.

3. A tuneable peptide hydrogel to model a defined metastatic site with optical clarity.

These models will initially be individually characterised and refined within the system, ensuring appropriate behaviour and ability to obtain detailed measurements of dynamic processes. They will then be combined into a broader model of tumour progression.

Development of brain tumour margin-on-a-chip model for treatment of tumour recurrence

Supervisors: Dr Christopher Chapman, Dr Agnes Nishimura

Developing therapeutic solutions for recurrent brain cancers, such as glioblastoma multiforme (GBM), is particularly difficult due to the lack of a relevant model of tumour resection and recurrence. There is an urgent need for development of new predictive in vitro models that allow for systematic and simultaneous investigation of the interactions between GBM cells, neurons, and astrocytes, during GBM recurrence to inform cancer therapy.

This project aims to engineer an organ-on-chip model that enables the co-culture of healthy neural cells with glioblastoma spheroids on a scale (millimetres) that microsurgical resection can be performed. After micro-resection, the regrowth of the remaining glioblastoma cells in the resection cavity will be monitored over time enabling quantification of recurrence characteristics and potential for screening novel therapeutic delivery. Three aims will be targeted in this project:

(1) Engineering a hydrogel-based microphysiological system capable of culturing healthy neural tissue and glioblastoma spheroids with access for microsurgical resection.

(2) Cellular characterisation of stages of recurrences at the on-chip tumour margin

(3) Embedding electronic sensors into the on-chip system tumour margin to enable testing of electrical treatment modalities such as tumour treating fields (TTFs) and monitoring physiological state changes during recurrence

This project will lead to improved understanding of phenotypic shifts in GBM cells over different recurrence timepoints in response to electrotherapies for GBM. Through a collaboration with Coherence Neuro, the successful candidate will be able to cross validate their findings with in vivo experiments using a novel electrotherapeutic device for GBM treatment.

Development of a dual-use skin-on-a-chip model for assessment of oncology drug toxicity

Supervisors: Prof John Connelly, Daniele Bergamaschi

Skin toxicity remains one of the most challenging dose-limiting side effects of oncology drugs, especially targeted therapies. Existing in vitro and animal models lack sufficient predictivity for clinical toxicity, hindering efforts to balance efficacy with safety in drug development. Development of validated human skin-on-chip platforms that mimic key toxicologic responses addresses this gap by providing industry and academia with more predictive tools, supporting safer and more effective anti-cancer drug discovery while minimising reliance on animal models. The overall aim of this PhD studentship is to develop a next-generation vascularised skin-on-chip platform that accurately replicates essential skin toxicity responses to cancer therapeutics.

The project will leverage QMUL’s state-of-the-art human skin models, which consist of a 3D printed skin equivalents containing keratinocytes, fibroblasts, endothelial cells, and resident macrophages. Building on this design, the proposed project will optimise the biophysical properties, perfusion and dosing of key drugs, establish robust toxicity readouts, and explore potential mechanisms of action. In addition, new technological advances will be implemented through the engineering of a dual-chip system that enables simultaneous prediction of drug toxicity in the skin-on-chip device and therapeutic efficacy in cancer models, thereby facilitating direct assessment of the therapeutic index and supporting optimised anti-cancer drug selection.

In collaboration with AstraZeneca, a major focus of the project will be to validate the skin-on-chip system with clinically relevant oncology agents to demonstrate correlation between in vitro readouts—target engagement, viability, proliferation, cytokine profiles, tissue integrity, immune activation—and clinical skin toxicity risk.

3D printing complex microenvironments for next generation musculoskeletal organ-chips

Supervisors: Prof Hazel Screen, Nidal Khatib

Organ-chip models offer exciting opportunity to unlock discovery science and pre-clinical testing, by providing more human-relevant models of disease. However, the design of appropriate niche environments within models to maintain physiological or pathological cell phenotype and function is crucial for their success.

Here we focus on the design of appropriate niche environments to capture the tendon-bone junction. The tendon-bone interface is a common site of painful, debilitating injury, where a vicious cycle of inflammation, tissue remodelling and interface stiffening drives further degeneration. We currently have no clear treatments for injury at the tendon-bone interface, but models to unpick and thus modulate the interplay between inflammation and tissue stiffening offer exciting potential for new drug targets.

In this project, we will work with the BIONOVA X 3D bioprinter (supplied by industrial partner CELLINK), to select and optimise printable hydrogels and light patterning approaches, to capture the tendon-bone stiffness gradient, and to integrating growth factor gradients which capture the biological gradient between the tissues. We will drive inflammation within the model, then utilise printing approaches to modulate the tissue stiffness at the junction, and explore how this impacts injury progression, driving mechanistic understanding of disease progression and identifying potential treatment targets for tendon-bone injuries.

CELLINK’s focus is in developing approaches to bioprint within organ-chip platforms. They will provide technical expertise, supervision and a placement focused on optimising the printing approaches, and will also work with us to explore how we translate these to support the development of a range of different models.

Development of spinal cord injury and repair-on-a-chip model

Supervisors: Prof Julien Gautrot, Dr Patrick Pallier

Spinal cord injury (SCI) affects over 4,400 people annually in the UK, with around 105,000 individuals currently living with the condition. These injuries often result in permanent disability, requiring long-term medical care, rehabilitation, and social support. With an average lifetime cost of £1.12 million per patient, SCI places a substantial burden on the NHS and wider healthcare system.

To support regenerative medicine approaches for SCI, human-based advanced in vitro models offer a promising alternative for predicting the efficacy and safety of biomaterials and cell therapies. However, suitable models of spinal cord damage and repair remain limited. This project aims to develop a novel model using 3D printed microfluidic platforms.

1. Chip engineering of spinal cord injury. Microfluidic chips will be designed to deliver reproducible compressive injury to motor neuron bundles. Using DLP printing, motor neuron spheroids will be guided through microchannels using chemokine gradients. A pneumatic chamber (microfabricated separately) will apply controlled compression. Chips will be characterised via electron and confocal microscopy, nanoindentation, and DMA.

2. Model Validation. Injury response will be assessed using bit.bio motor neuron bundles. Cell viability and apoptosis will be evaluated via live/dead assays and Annexin V/caspase markers. Axonal fate will be analysed through immunostaining and confocal imaging.

3. Repair Evaluation. Injured bundles will be treated with peptide amphiphile hydrogels with comparison to fibrin gels known to enable poor recovery potential. Regeneration will be assessed by axon connectivity (confocal microscopy/immunostaining) and calcium transport (fluorescence imaging).

Lung-on-a-chip model development for analysis of health effects of chemicals and pollutants in healthy and respiratory disease states

Supervisors: Dr Vito Mennella, Dr Emma Chambers

Preclinical evaluation of inhalation exposure to drugs, consumer products, and environmental pollutants still relies heavily on animal models, despite their limited translational accuracy and poor scalability. Human Air–Liquid Interface (ALI) airway cultures offer a more relevant in vitro alternative; however, their predictive performance is restricted by the absence of key biomechanical features of the respiratory tract, including cyclic stretch from breathing, directional airflow, and mucus transport. Conventional systems also rely on healthy epithelial cells, overlooking disease-specific mechanical and biochemical susceptibilities that can exacerbate toxic responses.

This project will develop an engineering-driven microphysiological lung-on-chip platform integrating controlled airflow, programmable mechanical deformation, and multi-cellular co-culture of epithelial, endothelial, and immune cells. Using primary and primary-like human bronchial epithelial cells, the platform will enable precise manipulation and quantification of biomechanical forces to determine how these parameters influence pesticide-induced respiratory toxicity. To increase physiological relevance, we will engineer disease-focused chip models, including Primary Ciliary Dyskinesia (PCD) and Asthma, capturing defects in motile cilia and altered mucus rheology arising from goblet cell metaplasia.

Building on preliminary ALI data from exposures to ten plant protection products, we will assess whether incorporation of dynamic flow, cyclic stretch, and disease-relevant states shifts toxic thresholds, alters epithelial barrier mechanics, and reshapes transcriptional stress responses. Outcomes will deliver mechanistic insight into how biomechanical cues regulate toxic response pathways and generate quantitative design principles for next-generation inhalation safety platforms.

Aims:

1. Engineer and validate a modular lung-on-chip platform modelling healthy and disease-relevant airway states.

2. Determine how cyclic mechanical stretch affects epithelial architecture and cell–cell junction organisation.

3. Quantify the impact of directional airflow and mucus transport on compound-induced toxicity using transcriptional, mucociliary clearance, and barrier integrity readouts.

Coaxial printing for an artery-on-a-chip model

Supervisors: Prof Thomas Iskratsch, Dr Christopher Chapman

Vascular smooth muscle cells (VSMCs) take a central role in the regulation of vascular tone, but also the ageing and/or disease associated arterial remodelling. In the normal arterial wall, VSMCs are contractile. However, in response to changing chemical and mechanical signals VSMCs take on alternative phenotypes that drive the arterial wall remodeling and disease progression. There is a lack of effective treatments for arterial disease, which in part is due to missing suitable models for studying the underlying cellular mechanisms and pathophysiology.

While different in vitro models have been proposed and used for studying VSMCs, these models were limited in the complexity of the tissue organisation and/or mechanical stimulation capabilities.

To overcome the limitations, this project will employ 3D printable conductive bioinks and coaxial 3D bioprinting to create artery-on-chip models that have (1) a in vivo like geometry with a lumen lined by endothelial cells (ECs), surrounded by a layer containing the VSMCs; (2) perfusability; (3) capability to electrically stimulate the arterial VSMCs (i.e. for depolarisation) to trigger cyclical contractions; (4) in-line sensing of the membrane potential;

The model will then be used to analyse the effects of electrical stimulation on phenotype of VSMCs and endothelial cells, as well to analyse membrane potential changes in response to flow and/or chemical stimulation for evaluation of membrane potential as marker for VSMC phenotype switching.

Overall, we anticipate the project to lead to the development of a novel artery-on-a chip model that can be used for effective drug discovery and toxicity testing

A digital twin for mechanics and mass transport of organ-on-a-chip technologies

Supervisors: Prof Y i Sui, Prof Martin Knight

Organ-on-a-chip (OoC) is a ground-breaking technology to simulate human organ function and physiology in vitro. These microfluidic devices replicate the dynamic environments of organs, making them critical for drug testing, disease modelling, and personalized medicine. However, one key challenge in OoC is understanding, predicting and controlling the mechanics, e.g., fluid forces and cell stresses, and transport of drugs and nutrients etc, to achieve accurate physiological mimicking. In particular, the state-of-the-art technologies, such as the Emulate S1 chip, often involves significant chip deformation, e.g., to mimicking breathing or pulsatile vasodilation, which lead to disturbances to fluid flow, mass transport, and cell dynamics that cannot be easily measured using conventional methods.

This PhD project will be build the world’s first digital twin for mainstream OoC platforms, enabling predictions of forces applied to cells, and transport of drugs, nutrients, and oxygen. These crucial information will be coupled with cell phenotypical changes, which will be monitored in real-time and fed back to the digital twin to online optimise the operational conditions, for the optimal physiologically relevant gradients, including shear stress, drug and nutrient.

The study will integrate computational modelling (e.g., CFD simulations of fluid mechanics and mass transport using in-house and commercial computational mechanics software) and experimental techniques (mechanobiology, fluorescence imaging). The student will be integrated with the Knight OoC group and will have access to both chip platforms and experimental data. The project team will work closely with world-leading providers of the OoC devices, including Emulate and CNBio.

Development of electrochemical biosensors for mapping hormone release in an adrenal gland-on-a-chip

Supervisors: Prof Steffi Krause, Prof Li Chan

We propose to develop a novel organ-on-chip platform capable of mapping the release of glucocorticoids (GCs) in-situ and in real time through electrochemical imaging. GCs are essential for life and necessary to respond to environmental stress, illness and changes in metabolism. Work (L Chan) is developing therapeutics for the treatment of diseases that affect the adrenal gland, but there are currently limited experimental tools to study human adrenal function and disease mechanisms. S Krause’s group has been working on photoelectrochemical imaging (PEI) of living cells monitoring parameters such as action potentials and ion concentrations. Through surface modification of the semiconducting PEI sensor substrate, analytes typically detected with electrochemical biosensors can be mapped with micron resolution and in real time.

The PhD aims to:

1. Develop a microfluidic system where one wall of the microfluidic channel is a PEI sensor with an aptamer modified surface capable of mapping local changes of different GCs.

2. Develop strategies to regenerate the sensor surface after GC binding to the aptamer and modify the surface to make it resistant to biofouling, e.g. through the growth of polymer brushes.

3. Integrate the microfluidic with the adrenal gland on chip model currently developed in L Chan’s group and investigate the local changes in extracellular GC concentration to study adrenal function and disease mechanisms.

This PhD will develop electrochemical imaging sensor capabilities that are applicable to many other organ-on-chip systems and to generate new technology focused ideas that will lead to future impact.

Development of high-throughput osteochondral models for screening osteoarthritis therapeutics

Supervisors: Dr Tim Hopkins, Prof Martin Knight

Osteoarthritis (OA) is the most common joint disease in the world, causing pain and disability for millions of people worldwide. OA involves and affects all joint tissues, but the osteochondral unit (cartilage and subchondral bone) are the most evidently impacted and therefore represent clear targets for treatment. However, there are still no disease-modifying treatments for OA. The search for new treatments is hampered by the lack of preclinical models. This project will involve the development and qualification of a suite of predictive in vitro models of the human osteochondral unit.

Osteochondral constructs will be generated using methods previously reported by our group. Human bone marrow mesenchymal stem cells (hBM-MSCs) will be encapsulated within hydrogels, along with hydrogel-embedded and media-delivered growth factors (e.g. TGFϐ and BMP2), to drive divergent osteogenic and chondrogenic differentiation into chondrocyte-like and osteoblast-like cells respectively. These models will be created using both a multi-well plate transwell system, and the MIMETAS OrganoPlateTM platform.

The project has been designed in collaboration with a major pharmaceutical company, based on their specific priorities, ensuring that the models developed have industrial utility and a direct pathway for adoption, translation and impact. Each model will balance the complexity required for physiological relevance and predictive power, with the need for reproducibility, high-throughput, and ease-of-use. The project will test the influence of the various components of the models including mechanical loading, the presence of additional tissue types (vasculature, synovium), immune cell incorporation, systemic vs localised inflammation, and matrix stiffness.

The student will benefit from belonging to a large, well-established research group, led by Professor Knight, while being primarily supervised by Dr Hopkins.

Advancing animal-free organ-on-a-chip with PeptiMatrix

Supervisors: Prof Martin Knight, Dr Tim Hopkins

The extracellular matrix (ECM) is a three-dimensional (3D), bioactive, instructive network that regulates cell behaviour through biochemical and biophysical cues. The ECM plays a crucial role in musculoskeletal (MSK) tissue development, function and dysfunction and should be considered an essential component in the design of Organ-on-a-Chip (OoC) models

Paradoxically, given the animal replacement potential of OoC, many of the hydrogels that are currently used to mimic the 3D ECM in MSK OoC systems are still animal-derived e.g. Matrigel™ and collagen type 1. This therefore represents a significant, but largely overlooked, source of animal use that necessitates replacement. In addition, animal-derived hydrogels are ill-defined, poorly-customisable, prone to batch-to-batch variability, and demonstrate insufficient mechanical properties. There is an urgent need for new, characterised, customisable and animal-free hydrogels for use in OoC models.

This project seeks to address this requirement using PeptiMatrix™, a fully synthetic and customisable peptide hydrogel platform designed for 3D cell culture. PeptiMatrix™ is available in a range of different stiffnesses, and with a range of functional augmentations. This studentship will evaluate the feasibility of using these formulations in a number of different OoC systems (Emulate, MIMETAS, BiomimX), and to model a number of MSK tissues (synovium, cartilage, bone). The project will assess the ability of these gels to maintain MSK cell viability and phenotype, transmit mechanical strain and ultimately to generate physiologically-relevant, engineered MSK tissues within OoC.

With technical and strategic consultancy provided by the PeptiMatrix™ team, this project could re-define 3D tissue microenvironments within MSK OoC. In addition, the applicability of these new materials and methodologies will not be limited to MSK tissues and has the potential for wide reaching impact across the OoC field.

Development of an adipose-cartilage-on-a-chip model to investigate the role of obesity in osteoarthritis

Supervisors: Dr Josephine Wu, Dr Stefaan Verbruggen

Osteoarthritis (OA) is an increasingly prevalent joint disease affecting 1 in 13 of the aging global population, characterized by cartilage degeneration leading to pain and disability. Obesity is a well-established risk factor for OA. Though the obesity-related risk of OA was traditionally attributed to increased mechanical loads on weight-bearing joints, emerging evidence highlights a key role of adipose tissue as a metabolic, biochemical, and inflammatory regulator in joint disease.

The overall goal of this project is to develop a multi-organ chip model to study the crosstalk between cartilage and adipose tissue in healthy and OA-like contexts. The project will aim to:

1. Establish healthy engineered models of cartilage and adipose, characterizing them through histological and biochemical/molecular analyses

2. Optimize their integration into a perfused microphysiological system, allowing dynamic communication via circulating soluble factors.

3. Induce an OA-like state to study the influence of the adipose tissue compartment on disease progression, particularly degeneration of cartilage matrix and upregulation of inflammatory cytokines.

This work will leverage the ongoing research of Dr Wu on cartilage tissue engineering and biofabrication, the expertise of Dr Verbruggen on organ chips and mechanobiology, paired with the microfluidic platforms and adipose tissue models of industry partner Cherry Biotech. The resulting bioengineered model will provide a preclinical platform to study the effects of obesity in joint disease and to test novel OA therapeutics, ultimately advancing our understanding of metabolic health and musculoskeletal degeneration.

Development of an immune-infiltrated adipose tissue-on-a-chip model for interactions between inflammation and dysfunction

Supervisors: Dr Claire Villette, Dr Stefaan Verbruggen

While healthy adipose tissue (AT) is key for energy storage and heat generation, its dysfunction contributes to the development of metabolic and cardiovascular diseases as well as cancer. AT dysfunction is characterized by chronic inflammation whereby immune cells infiltrate the tissue and induce further metabolic disturbances, contributing to a vicious cycle of AT dysfunction.

This exciting PhD studentship will develop new organ-on-chip models to recapitulate this vicious cycle of AT dysfunction, and couple them to a digital twin. The student will start by developing an advanced multicellular model of human AT, before introducing macrophage infiltration via state-of-the-art microfluidics. The student will then use this setup to inform the development of a computational model capturing the interactions between macrophage behaviour and AT dysfunction, leveraging the synergy between experimental and computational models.

Overall, this project will provide clinically-relevant in-vitro/in-silico disease models to investigate therapeutic avenues to counter AT dysfunction. Applications include obesity/diabetes disease modelling, dual-organ investigations (e.g: adipose-liver, adipose-cartilage interactions), as well as studies on bone-marrow fat influence on bone cancer.

The project is supported by our partnership with the organ-chip company, CN-Bio, and will use their commercial state-of-the-art multi-organ platform available within the Centre. This studentship also includes the option of a placement in CN-Bio's laboratories in Cambridge. The student will be part of a large multi-disciplinary organ-chip research group and will be supported by 3 post docs working on a new EPSRC grant in this area of organ-chip technology (EPSRC grant: Organ-chips for accelerated deployment of new medicines)

Human vascularised tendon construct-on-a-chip model for the study of tendinopathy

Supervisors: Nidal Khatib, Prof Hazel Screen

Tendon injury and tendinopathy are painful and debilitating conditions affecting athletes, workers and ageing populations alike. Despite the prevalence of tendon disorders, therapeutic development has been hindered by a lack of physiologically-relevant models that reflect tendon’s unique, hierarchical tissue organisation and mechanobiology. Organ-on-a-chip technologies now offer an opportunity to transform tendon research by recreating the native mechanical, structural and cellular environment of human tendon in vitro.

This project will develop a next-generation, stratified tendon construct using the Emulate Open-Top Chip-A1 platform, incorporating distinct niches with tailored stiffness, composition and topology for each tendon region. Building on our recent advances in material science, mechanobiology and microphysiological engineering, these constructs will be integrated into a chip system enabling controlled flow, vascular simulation and mechanical loading.

The work will involve construction and optimisation of multi-layered gel-nanofiber substrates and validation of mechanical performance using biomechanical testing techniques. Chips will be seeded with primary human tendon cell populations and biological exploration will utilise biochemical, molecular biology and imaging techniques. The final system will serve as a robust human-relevant model for studying tendon physiology, injury mechanisms and therapeutics, and has potential to become a benchmark tool for future research.

The project will ntegrate into the well-established research group of Prof Hazel Screen. External supervision and strategic input will be provided by Emulate, and the studentship includes the opportunity to undertake a placement with Emulate in Boston to gain hands-on experience with their activity.

Targeting inflammatory pathways in asthma utilising an alveolar lung-on-a-chip model

Supervisors: Dr Emma Chambers, Prof John Connelly

Asthma is a chronic lung condition and currently there are 7.2million people in the UK with the disease. Asthma is an inflammatory disease of the lung which results in airway remodelling, loss of elasticity, airway hyperresponsiveness and mucus hyperplasia. Asthma pathology is driven by a combination of lung stromal cells such as epithelial cells as well as lung resident immune cells such as macrophages, mast cells and T cells.

Currently scientists study asthma either using mouse models of disease or static air-liquid-interphase culture systems – limitations to both these models mean they do not fully recapitulate human asthmatic lung mechanobiology. Therefore, there is a clear unmet need to develop more physiological lung models which model the human asthmatic lung including, relevant biophysical cues and immune cells. Preliminary data has shown that the EMULATE alveolar chip model recreates the human lung most effectively, with immune cells flowing through the endothelium and stretch caused by breathing recreated.

The overarching aim of this project is to engineer a novel asthma model using the EMULATE alveolar-chip platform.

To achieve this the following experimental aims are proposed:

1. Adapt the EMULATE alveolar-chip to model asthma, utilising asthma patient cell lines and disease mimicking biophysical cues (impaired stretch and fluid flow).

2. Incorporate myeloid cells into the model to make the asthma EMULATE model immune responsive.

3. Investigate the interplay between mechanical cues and immune cells in asthma disease severity/progression.

4. Test anti-inflammatory drugs using the immune responsive asthma EMULATE model to determine if inflammatory pathways are reduced.

Overall, this project will establish a novel asthma lung on a chip model with an immune cell component which can be used to test novel anti-inflammatory therapies. In addition, the studies will provide new insight into the mechanobiology of asthma progression