PhD Student in the McSorley Lab @ University of Dundee.Division of Cell Signalling and Immunology

As part of my EASTBIO PhD, I was required to plan and conduct a "Professional Internships for PhD Students" (PIPS).In March 2022, I moved to Tucson, Arizona to work with the Sonoran Desert Network (an Inventory and Monitoring Network within the National Park Service) and helped develop a protocol for the isolation of environmental DNA. Attempting to confirm the presence of elusive wildlife (e.g. Jaguars) but also monitor diseases (e.g. Chytrid Fungus, Ranavirus) which threaten native species of the Sonoran Desert.More on the eDNA protocol and my time in Arizona can be found on their website. (linked below)or on the EASTBIO PIPS website (linked below)

In my current post, I have been working within the Maizels Lab at the University of Glasgow. My research focusses on understanding various aspects of the interactions between parasitic helminths and the host immune system. How parasites regulate and/or evade the immune response and the therapeutic potential of the parasite’s immunomodulatory products. Recently, I have been investigating the relationship between parasitic helminths and the poorly understood tuft cell population in the small intestine. Tuft cells appear to have a strong influence on the downstream response to infection; capable of guiding the adaptive type 2 immune response. Understanding the cellular and molecular mechanisms behind this response could help further our understanding of gastrointestinal diseases such as colitis, colorectal cancer and more. This work involves using animal models of disease to study the immune response to infection. Data is gathered through various modern techniques such as: flow cytometry, cell sorting, ELISA, cell culture, metabolomics, immunohistochemistry, molecular techniques (PCR, qPCR, RT-PCR, RT-qPCR) and genome sequencing. I have benefited greatly from being involved in such a multidisciplinary group; comprised of immunologists, parasitologists and molecular biologists. Through this position I have greatly improved my skills in animal research, experimental design and interpretation of results.http://maizelslab.org/

The role of γδ T cells in continuing Cystic Fibrosis inflammation Dr Emily Gwyer Findlay / Centre for Inflammation ResearchMSc Research Project - March 2018–Sept 2018 Cystic Fibrosis (CF) is a recessively-inherited, autosomal genetic disorder which dramatically reduces the life expectancy of affected individuals. Early colonisation of the lungs by pathogenic bacteria results in non-resolving inflammation in CF airways. Respiratory failure becomes inevitable and will cause mortality in 95% of sufferers. Neutrophils have long been considered the drivers of pathology, however, other cellular and molecular mechanisms exist which initiate and sustain the inflammatory response. γδ T cells exist in large numbers within the lung and acts as an important first-line of defence. These lymphocytes are early sources of pro-inflammatory cytokines such as TNF-α, IFN-γ and IL-17A; all of which are capable of recruiting effector cells, initiating an anti-bacterial response, and driving inflammation. Surprisingly, the role of γδ T cells during CF inflammation remains completely unknown.In this study, we questioned the role of γδ T cells during chronic CF inflammation and how they may influence the inflammatory environment. Of particular interest, how γδ T cells interact with neutrophils and respond to the products released as neutrophils degranulate, driving pathology of the lung. The project involved the analysis of human samples donated from CF patients; immune populations were phenotyped using flow cytometry, ELISA, cell culture and more.

The role of IL-33, an early epithelial alarmin, in parasitic helminth infection. Dr Henry McSorley / Centre for Inflammation ResearchMSc Research Project - Sept 2017–March 2018 In this postgraduate research project, we focused on the actions of Interleukin-33 (IL-33), a member of the IL-1 family, which functions primarily as a potent "alarmin" cytokine. IL-33 is crucial for alerting the immune system of local tissue damage. The cytokine is released from epithelial cells under necrotic conditions, recognized by local effector cells and initiates a type 2 immune response which serves to protect host from injury, insult and infection. The cytokine is actively suppressed during infection with the helminth H. polygyrus and is important for resistance to helminths. Current interest in IL 33 has been invigorated by its participation in the activation and expansion of ILC2, eosinophils and Treg cell populations. With such an important role in the immune system, IL-33's involvement in responses to infection, allergy and autoimmune diseases potentiates the cytokine as an attractive target for therapeutic intervention. Cell culture, western blotting and ELISA were all used to assess IL-33 function in vitro. Biopsies from both ruminant and murine tissues allowed further analysis - ex vivo. Additionally, using infection with parasites - H. polygyrus and N. brasiliensis – we assessed the in vivo role of IL-33 during tissue repair, inflammation, and fibrosis (histology, flow cytometry, ELISA).

The role included the designing and ongoing development of database systems, aiming to improve the efficiency of the company's data processing. System monitoring and improving database performance and capacity, and planning for future expansion requirements. As well as planning, co-ordinating and implementing security measures to safeguard the database. Analysis and replacement of less-efficient systems.