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  Investigating the mechanisms of fungal induced airway damage and biomarker production in asthma

   School of Science, Engineering and Environment

  Dr Sara Namvar, Dr Arijit Mukhopadhyay  Applications accepted all year round  Self-Funded PhD Students Only

About the Project

Information on this PhD research area can be found further down this page under the details about the Widening Participation Scholarship given immediately below.

Applications for this PhD research are welcomed from anyone worldwide but there is an opportunity for UK candidates (or eligible for UK fees) to apply for a widening participation scholarship.

Widening Participation Scholarship: Any UK candidates (or eligible for UK fees) is invited to apply. Our scholarships seek to increase participation from groups currently under-represented within research. A priority will be given to students that meet the widening participation criteria and to graduates of the University of Salford. For more information about widening participation, follow this link: [Scroll down the page until you reach the heading “PhD widening participation scholarships”.] Please note: we accept applications all year but the deadline for applying for the widening participation scholarships in 2024 is 28th March 2024. All candidates who wish to apply for the MPhil or PhD widening participation scholarship will first need to apply for and be accepted onto a research degree programme. As long as you have submitted your completed application for September/October 2024 intake by 28 February 2024 and you qualify for UK fees, you will be sent a very short scholarship application. This form must be returned by 28 March 2024. Applications received after this date must either wait until the next round or opt for the self-funded PhD route.


Project description: Respiratory diseases such as asthma are a major global cause of morbidity and mortality. For instance, according to European Union estimates, asthma and COPD alone cost the economy approximately 40 billion Euros and responsible for around 200,000 deaths annually. This highlights that despite our best effort, findings are not currently translating from bench-to-bedside effectively. We have developed a number of respiratory cell culture based models suitable for the assessment of airway damage and biomarkers of disease. This project will involve the development of a 3D airway model, comprising primary asthmatic airway epithelial cells cultured at air-liquid interface (ALI) in the presence of fibroblasts. Our previous research demonstrated an important role for fungal proteases and Endothelin-1 signalling mechanisms. Using this novel 3D model, this project will unravel the detailed mechanisms by which fungi drive airway scarring responses and biomarker production. The validity of key biomarker discoveries made in vitro, will be assessed in asthmatic patient samples. This project will involve the use of cutting-edge imaging techniques, in vitro physiological assessments and a wide range of molecular techniques. For biomarker discovery with a potential of non-invasive usage, we will use isolation and characterisation of small extracellular vesicles and investigate their cargo. We will particularly focus on microRNA cargo as a biomarker including any epi-transcriptomic changes.

Biological Sciences (4)


Namvar, S , Labram, B, Rowley, J and Herrick, S 2022, 'Aspergillus fumigatus —host interactions mediating airway wall remodelling in asthma' , Journal of Fungi, 8 (2) , e159.
Namvar, S, Rowley, J, Gago, S , Labram, B, Bowyer, P, Richardson, MD and Herrick, SE 2021, 'Differential proinflammatory responses to Aspergillus fumigatus by airway epithelial cells in vitro are protease dependent' , Journal of Fungi, 7 (6) , e468.
Namvar, S, Labram, B , Hussell, T and Herrick, SE 2019, 'Endothelin-1 mediates Aspergillus fumigatus induced airway inflammation and remodelling' , Clinical and Experimental Allergy, 49 (6) , pp. 861-873.
Namvar, S , Warn, P, Farnell, E, Bromley, M, Fraczek, M , Bowyer, P and Herrick, S 2015, 'Aspergillus fumigatus proteases, Asp f 5 and Asp f 13, are essential for airway inflammation and remodelling in a murine inhalation model' , Clinical and Experimental Allergy, 45 (5) , pp. 982-993.

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