Professor Julie Morrissey

Supervisor Details

Contact Details

Department of Genetics, Genomics and Cancer Sciences, University of Leicester

Scientific Background

Research Interests

I am interested in how bacteria adapt to different environmental conditions to change their behaviour to increase colonisation and infection. I work with several bacterial species (Staphylococcus aureus and Moraxella catarrhalis) investigating stress adaptation mechanisms, including particulate matter (black carbon, brake dust) and metals (copper). Our team also investigate the impact of pollutants on host-bacterial interaction using human epithelial infection models showing that direct interaction of pollutants with bacterial pathogens increases infectivity and interaction with human respiratory cells. I am very enthusiastic about supporting my students and my previous students have gone on to academia, Food Standards Agency, Foreign Office, industry, aerospace engineering and several are PDRAs in our team or with collaborators.

Research Groups

Microbial Sciences and Infectious Disease Centre (LeMID)

NIHR Health Protection Research Unit in Chemical Threats and Hazards

Supervision Style

In three words or phrases: supportive, collaborative, outcome-oriented

Provision of Training

We prefer to take responsibility for your technical training as a team with myself and my experienced post docs/PhD students at first, leading to more independence later.

Progression Monitoring and Management

I like to be kept up to date, and will expect to see evidence of method development/data generation results on a weekly basis. If these progression criteria are not met we will always discuss a plan of action together.

Communication

I am happy to discuss issues that are impacting your ability to fulfil your potential or my/our expectations.

Meetings

PhD Students can expect scheduled meetings with me at least once per week. These meetings will be face-to-face. I have an open door policy, but my pattern of being contactable for an instant response is not predictable.

Work Patterns

Work in my lab requires being present on site (be it in a laboratory or at a field site) during the core hours of 10am - 5pm (or a subset if working part time).

Notice Period for Feedback

I need at least 2 weeks' notice to provide feedback on written work of up to 5,000 words.

MIBTP Project Details

Primary supervisor for:

How does air pollution increase bacterial pathogens' antibiotic resistance and colonisation?

See the PhD Opportunities section to see if this project is currently open for applications via MIBTP.

Please Note: The main page lists projects via BBSRC Research Theme(s) quoted and then relevant Topic(s).

How does air pollution increase bacterial pathogens' antibiotic resistance and colonisation?

Secondary Supervisor(s): Dr Jo Purves

University of Registration: University of Leicester

BBSRC Research Themes:

Understanding the Rules of Life (Microbiology)

Project Outline

Particulate pollutants, a key component of air pollution, are increasing through wildfires and climate change. Particulate pollutants cause increased respiratory and infectious diseases. However, how these physical pollutants interact with pathogens at the ecological and physiological level is unclear.

Importantly we found that particulate pollutants alter bacterial gene responses causing increased antimicrobial tolerance and ability to infect. The response is widespread with different bacterial species showing similar phenotypic responses but interestingly each species has a unique transcriptional response.

We still do not understand how particulate-bacterial interaction changes gene expression. Our hypothesis is that particulates interact with the bacterial cell surface stimulating a novel cell envelope stress response to counteract minor damage and subsequently increase colonisation. We aim to use our extensive phenotypic, transcriptomic and proteomic data from Staphylococcus aureus, Haemophilus influenzae and Moraxella catarrhalis to test the hypothesis and establish how particulate pollutants stimulate stress responses to increase colonisation and antimicrobial tolerance, with an aim to identify novel therapeutic targets.

Objectives:

Determine how particulate pollutants induce cell envelope stress responses.
Establish the key regulatory mechanism that promote biofilm formation and antibiotic resistance.
Identify key targets to explore as novel therapeutics.

Research plan:

The methodologies used will include molecular microbiology, ‘omic analysis, human tissue culture and advanced imaging microscopy techniques. The team includes microbiologists, clinicians, engineers, and government agencies e.g UKHSA and EA. This is an exciting, inter-disciplinary project with environment and healthcare implications and opportunities.

doi./10.1111/1462-2920.13686; doi:10.1111/1462-2920.16076, doi./10.1038/s41522-024-00632-3

How does copper increase antibiotic resistance and ability to cause infection?

See the PhD Opportunities section to see if this project is currently open for applications via MIBTP.

Please Note: The main page lists projects via BBSRC Research Theme(s) quoted and then relevant Topic(s).

How does copper increase antibiotic resistance and ability to cause infection?

Secondary Supervisor(s): Professor Joan Geoghegan

University of Registration: University of Leicester

BBSRC Research Themes:

Understanding the Rules of Life (Microbiology)

Project Outline

Excess copper is highly toxic and forms part of the host innate immune system’s antibacterial arsenal, accumulating at sites of infection and acting within macrophages to kill engulfed pathogens.

All bacteria possess mechanisms to resist copper toxicity. The importance of bacterial copper resistance is evidenced by epidemic methicillin resistant Staphylococcus aureus (MRSA) acquisition of additional resistance mechanisms that confer copper-hyper resistance causing increased resistance to killing by macrophages and increased S. aureus infectivity.

Importantly our recent data show that subinhibitory copper functions as a regulatory signal, triggering coordinated transcriptional and metabolic remodelling that potentiates S. aureus fitness in the host. Copper alters expression of antibiotic resistance, virulence and immune evasion factors and alters the interaction of S. aureus with human epithelial cells.

Our hypothesis is that copper acts as an environmental signal to drive differential metabolic and physiological changes to potentiate S. aureus resilience to colonise multiple niches. However, the regulatory mechanisms involved and importance of copper homeostasis in clinical S. aureus carriage and disease isolates is unknown.

Aim is to:

Identify the regulatory mechanisms critical for increased colonisation and antibiotic resistance.
Determine importance of copper homeostasis mechanisms for clinical S. aureus isolates.
Identify and explore novel therapeutic targets.

The methodologies used will include molecular microbiology, ‘omic analysis, human tissue culture and advanced imaging microscopy techniques. The team includes microbiologists, clinicians, and government agencies e.g UKHSA and Professor Joan Geoghegan, University of Birmingham. This is an exciting, inter-disciplinary project with environment and healthcare implications and opportunities.

Environ Microbiol. 20:1576-1589; MBio. 2018 9. pii: e00550-18; BIORXIV-2026-732922v1-Morrissey