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Dr Cedric Berger

Dr Cedric Berger

Senior Lecturer, Associate Theme Lead for Immunology, Infection and Inflammation

School of Biosciences

Email:
bergerc3@cardiff.ac.uk
Telephone:
+44 (0)29 2087 4829
Location:
Room W/2.03, Sir Martin Evans Building, Museum Avenue, Cardiff, CF10 3AX
Available for postgraduate supervision

I am a senior lecturer within the Microbiomes, Microbes and Informatics (MMI) group within the Cardiff School of Biosciences. My group is studying the interaction between enteric pathogens and their hosts with a specific emphasis on Enterohemorrhagic (EHEC), Enteropathogenic (EPEC) and Diffusely adherent Escherichia coli (DAEC).  Our research covers the biology, immunology and the prevention of enteric diseases. We are focusing on the molecular mechanisms that occur within infected epithelial cells of the intestine (Figure 1). Infection may lead to abnormal responses associated with chronic inflammation (inflammatory bowel diseases) and colonic cancers.

My group is associated with Cardiff Research into Infection and Parasites in Ecological Systems (CRIPES) and with 
Water Research Institute.

You can also find our publication information on ResearchGate and a verified record of journal reviews on Publons. Please, do not hesitate to follow me on Twitter.

For almost 20 years I have been interested in bacterial infection and methods to prevent them. My PhD project at University Paris Sud at the faculty of Pharmacy in France focused on the interaction between Diffusely adherent Escherichia coli and the human epithelial cells. In 2006, I then moved to Imperial College London and developed my expertise on biomedical microbiology focusing on the human pathogens Enteropathogenic and Enterohemorrhagic E. coli and the mouse-restricted pathogen Citrobacter rodentium. In September 2018, I joined Cardiff School of Biosciences, Cardiff University, as a Senior Lecturer, to carry on my work on pathogenic bacteria.

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I carry out a range of teaching from year 1 to final year undergraduate, and the supervision of final year and postgraduate MRes project students.

My current teaching includes contributions to:

  • BI1001: Skill for Science - Problem solving in Biology.  
  • BI1003: Organisms and Environment - An introduction to diarrheal diseases
  • BI2332: Concepts of Disease - a practical on outbreaks of infection and lectures on Cholera and Salmonellosis
  • BI3155: Infection biology and epidemiology - lectures on host responses to infection.

Research

We are working on several host-bacterial pathogen systems combining a wide range of techniques and approaches from in-vitro cell assays to in vivo models. The aim of my group is to understand the molecular mechanism of bacterial virulence factors and identify their targets in the host.

Modulation of immune response

Escherichia coli is the major constitute of the aerobic gut microbiota. However, acquisition of virulence determinant by horizontal gene transfer led to the evolution of pathogenic E. coli clones. Pathogenic strains are divided into ExPEC (causing extra intestinal infection) and diarrhoeal E. coli, which are sub-divided into six categories: diffusely adherent (DAEC), entero-toxigenic (ETEC), -aggregative (EAEC), -invasive (EIEC), -pathogenic (EPEC) and -haemorrhagic (EHEC). Although EPEC and EHEC exhibit differences in their host specificity, epidemiology, virulence and disease symptoms, they colonise the gut mucosa of their respective hosts via attaching and effacing (A/E) lesions. A/E lesions are characterised by effacement of the brush border microvilli and intimate bacterial attachment to the enterocyte membrane (Figure 2). The ability to induce A/E lesions and colonize their hosts depend on a type III secretion system (T3SS) that injects effectors into colonic intestinal epithelial cells (IECs). Once injected, the effectors subvert processes involved in innate immune responses, cellular metabolism, and oxygenation of the mucosa. We recently reported that one of these effectors modulates the recruitment of neutrophils during mouse model of EPEC infection (Citrobacter rodentium). We are now focusing on other effectors that may target key signalling pathways that lead to the expression of cytokines.

Disease prevention

Different vaccinations, composed of virulence factors, DNA-based, attenuated bacteria or bacterial ghost against EPEC and EHEC, have been trialled in animals with mixed success. Vaccination against Intimin decreases EPEC colonization in the rabbit model. Vaccination targeting EspA, Tir and Intimin alters EHEC colonization in cattle but did not completely inhibit it. This vaccination was one of the two commercially available against EHEC, EconicheTM, but its production has stopped. The main problems of all these vaccinations is the diversity of the target among EPEC and EHEC suggesting that a single approach will not work.

The aim of this project is to develop a vaccine that could be used in children to prevent disease development or in animals to alter the colonization of EPEC and EHEC using C. rodentium, a mouse specific pathogen, used to study EPEC and EHEC infection in vivo as it shares the same virulence factors.

Current members of the Research Group

Postgraduate research students

Rema El-Turke – Mres student working on actin cytoskeleton reorganisation

Jack Alderton – Mres student working on actin cytoskeleton reorganisation

Undergraduate research students

Habiba Saif – Final year project student working on interferon signalling

I am currently supervising 2 postgraduate MRes project students:

  • Rema El-Turke
  • Jack Alderton

And one PhD student: