Keynote Speakers

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Robin Warren,

Australian pathologist & Nobel Laureate

Australian pathologist and Nobel Laureate, Robin Warren, needs no introduction. He won the Nobel Prize in Medicine in 2005 for the discovery of the bacterium Helicobacter pylori and its role in the gastritis and peptic ulcer disease. Warren’s life took a major turn when he noticed an unexpected bacterial growth in the gastric biopsy of a patient. Determined to find out the cause of it, he ventured forth and began extensively studying the same along with Barry Marshall. It took the duo seven years to eventually establish the presence of bacterium Helicobacter pylori as the major cause for peptic ulcer. Interestingly, their finding and research was not accepted by the scientific society which rebuffed the fact that bacteria of any kind could survive in the acidic environment of the stomach. It was only later on that the global community accepted the duo’s finding and thus awarded them with the prestigious Nobel Prize. His discovery has allowed for a breakthrough in understanding a causative link between Helicobacter pylori infection and stomach cancer.

Discovering Helicobacter
Discovering Helicobacter
Before the 1970’s, well fixed specimens of gastric mucosa were rare. Then the flexible endoscope was introduced. This enabled gastroenterologists to take numerous well-fixed small biopsies from the stomach. Gastric histology and pathology were clearly demonstrated. Whitehead accurately described it in 1972, including a feature he termed ‘active’ gastritis. This involved only the superficial gastric epithelium, with polymorph infiltration and epithelial cell distortion.
In June 1979 I was examining a gastric biopsy showing chronic inflammation and the active change. A thin blue line on the surface showed numerous small curved bacilli. These were clearly visible with a Warthin Starry silver stain. They appeared to grow on the surface of the foveolar epithelial cells.
Over the next two years I collected numerous similar cases. The changes were often much milder or more focal than the original biopsy, but the main features were usually similar, with chronic gastritis and usually some of the active change. These features could show considerable variation, from near normal to severe.
In 1981 I met Barry Marshal and we completed a clinico-pathological study of 100 outpatients referred for gastroscopy. There was little relation between the infection and the patients’ symptoms. Peptic ulcers, particularly duodenal ulcers, were very closely related to the infection. We cultured Helicobacter pylori.
In 1986, with Marshall et al, I studied the effect of eradication of H pylori on the recurrence of duodenal ulcer. I graded the gastritis (0 – 36) using the features seen with active gastritis. The range was 15 – 35 before treatment. After eradication of H pylori, this changed to 5 – 20 within 2 weeks. This provides powerful evidence that H pylori causes the active change.
Duodenal ulcer usually occurs in the duodenal cap. Gastric mucosa normally extends through the pylorus. In this study, the proximal border of all ulcers was either definite gastric mucosa, or scarred and consistent with a gastric origin. This suggests duodenal ulcer is either actually a distal pyloric ulcer or gastro-duodenal. It may well arise in the damaged, inflamed and infected mucosa in the position of maximum stress – the lip of the pyloric sphincter.

Thomas F. Meyer,
Max Planck Institute for Infection Biology, Department of Molecular Biology, Berlin

Thomas F. Meyer is Director of the Department of Molecular Biology at the Max Planck Institute for Infection Biology and Senior Professor at the Charité University Medicine in Berlin. His background is in molecular biology as well as the molecular and cellular biology of infections. His work is rooted in basic biological questions and led to several seminal discoveries in the areas of molecular genetics, microbiology, cell biology and cancer biology. Infectious agents have always been at the centre of his work. Following the recent progress in the development of powerful enabling techniques in genomics and cell biology, his focus also turned towards questions of particular clinical relevance, with an emphasis on the relationship between chronic bacterial infections, inflammation and human cancer.

 This current area of research stems from the notion that the mucosa is the major crossing point for molecular interaction between our body and the environment. This is where most pathogens initiate their infections and where our defence system is challenged to rapidly counteract any approaching assaults. Repeated or persistent onslaughts of this kind, however, tend to cause permanent damage to our epithelium and, not surprisingly, the mucosal epithelium is the site most prone to carcinogenesis, a consequence of enhanced mutagenesis, inflammation and cell proliferation. Several clear links have been noted between chronic bacterial infections and carcinogenesis; however, the underlying mechanisms of this likely fatal relationship are still sparsely understood. Exploring these mechanisms promises to pave the way towards better prevention and treatment of chronic infectious diseases and resulting sequels.

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Inflammation and persistence as hallmarks of Helicobacter pylori infections and starting points of gastric carcinogenesis

As one of the most successful pathogens Helicobacter pylori colonizes the stomachs of about 50% of the world’s population. It is implicated in mild to severe gastric and duodenal disease, most importantly though, gastric carcinogenesis. The bacterium has a long history of association with humans, reaching back for ~600,000 years, an immense time span that led to an intimate adaptation between pathogen and host. It is probably a consequence of this co-evolution that H. pylori has the ability to persist life-long in the gastric mucosa and this persistence endures despite the immense inflammatory response provoked by the infection.

 My laboratory has recently identified a key inflammatory factor of H. pylori released via the pathogen’s type 4 secretion system (T4SS). It is an ADP-heptose that functions as a building block of LPS synthesis and is recognized in the mucosal epithelium by the novel pattern recognition kinase Alpk1. Phosphorylation of TIFA then leads to an activation of NF-kB and pro-inflammatory chemokine release. The following recruitment of immune cells to the infected sites which mount vivid Th1 and Th17 responses seems to somewhat dampen the infection, however, is unable to eliminate the pathogen. Our recent work identified the underlying mechanism of this crucial failure: H. pylori possesses a glucosyl-a-transferase, which facilitates the extraction of host cell cholesterol from the epithelial membranes. Concomitantly, lipid rafts are effectively degraded rendering host cells unable to respond to a number of inflammatory cytokines, such as IFNg and IL22. Resulting failure of JAK/STAT activation and downstream transcriptional signaling thus prevents the release of highly effective antimicrobial peptides.

 This highly intriguing mechanism of bacterial persistence likely is a driving force by which adaptive mutations occur in the stomach mucosa, which, on the one hand, appear to preserve the stomach from greater damage yet, on the other hand, drive gastric pathology towards the development of pre-cancerous lesions and gastric adenocarcinoma. This novel concept of gastric carcinogenesis will be discussed in my presentation in more detail.

Jorge E. Galán,
D.M.V., Ph.D.

Lucille B. Markey Professor of Microbiology
Chair, Department of Microbial Pathogenesis
Yale University School of Medicine

Dr. Jorge E. Galán is the Lucille B. Markey Professor of Microbiology, Chair of the Department of Microbial Pathogenesis and Professor of Cell Biology at the Yale University School of Medicine. Dr. Galán is the recipient of numerous honors and awards including the the Hans Sigrist and the Robert Koch and the Prizes and membership of the USA National Academy of Science. Dr. Galán has made numerous contributions to the field of bacterial pathogenesis pioneering the study of the cell biology of infection and the mechanisms of pathogenesis of the enteric pathogens Salmonella spp. and Campylobacter jejuni as well as the mechanisms of protein secretion in bacterial pathogesn.

Brendan Wren,
London School of Hygiene and Tropical Medicine

Brendan Wren studied for a PhD in Physical Chemistry and published seminal papers on the effect of ionizing radiation on DNA. He then changed subject discipline and took a Microbiology position at St Bartholomew’s Hospital, London to study Helicobacter and Campylobacter.

 In 1999 he moved to the London School of Hygiene and Tropical Medicine and was awarded a chair in Microbial Pathogenesis. His primary research interest includes the molecular characterization of bacterial virulence determinants and the evolution of virulence. Much research has focused on bacterial glycostructures, including the characterization of lipo-oligosaccharides, capsular polysaccharides and glycosylation systems. Of note, basic research on Campylobacter glycosylation systems has facilitated glycoengineering in E. coli. To date, the major application of this technology is the construction of more affordable recombinant glycoconjugate vaccines.

He has published over 320 scientific papers including over 100 on Helicobacter and Campylobacter species relating to genomics, epidemiology and pathogenesis.

Solving the Campylobacter Conundrums - a look back in anger
Solving the Campylobacter conundrums – a look back in anger

Brendan Wren, London School of Hygiene and Tropical Medicine

In the past three decades the reported incidence of Campylobacter infection has steadily risen in the developed world and the incidence in low resource countries is poorly explored. Despite its prevalence, importance and intense research there remains many unanswered questions regarding the organism and disease. This can be largely attributed to the Campylobacter conundrums.

1. How can such a weedy organism that can’t survive in the ambient atmosphere and doesn’t transfer from person to person, be the leading cause of bacterial enteritis worldwide?
2. How does an organism without readily identifiable toxins cause diarrhoea?
3. How do avians tolerate trillions of Campylobacters, but humans can’t stomach a 100?
4. Why does Campylobacter infection present differently in developed countries (bloody diarrhoea) compared to low resource countries (watery diarrhoea)?

This presentation will explore the progress made in attempting to answer these conundrums using genetic, genomic, molecular and cellular approaches. Finally, the presentation will review the most promising interventions to reduce this enigmatic pathogen from the food chain.

Prof Steffen Backert 
Friedrich-Alexander University Erlangen-Nuremberg

My group is working in the field of Microbial Pathogenesis for more than 20 years. Our major research interest is the investigation of molecular signalling pathways during host-pathogen interactions in enteric infections such as that of Helicobacter pylori and Campylobacter jejuni. We focus on the identification of new bacterial virulence factors (secreted or injected), which could represent potential novel targets for therapeutic intervention. During recent years, my team made significant progress in characterising the genetics and infection cycles of the gastric pathogen and class-I carcinogen H. pylori and C. jejuni, analysing its pathogenicity mechanisms and host signal transduction pathways using modern cell biology and biochemical approaches.

One highlight of our research was the discovery that the H. pylori virulence factor CagA is translocated by a type-IV secretion system (T4SS) into mammalian host cells, where CagA targets tyrosine kinases and induces oncogenic signalling processes. In addition, we discovered the first host cell receptor of a bacterial T4SS, integrin-β1. We also identified the first eukaryotic kinase for a bacterial effector protein (Src for CagA) and described the first bacterial factor, which mimics a human extracellular matrix protein in vitro and during infection in vivo (H. pylori CagL as a mimetic of fibronectin). Finally, we are working on a newly discovered secreted factor, serine protease HtrA. HtrA interacts with components of intercellular tight junctions (Occludin and Claudin-8) and adherens junctions (E-cadherin), followed by the T4SS-pilus contacting integrin-based focal adhesions to disrupt and transform the epithelial cell layer in the human stomach.

Type IV secretion and pathogenesis of Helicobacter pylori
Steffen Backert

Department of Biology, Division of Microbiology, Friedrich Alexander University Erlangen-Nuremberg, Staudtstr. 5, D-91058 Erlangen, Germany

Many Gram-negative and Gram-positive bacterial pathogens harbour type IV secretion systems (T4SSs), which translocate virulence factors into host cells to hijack cellular processes for multiple purposes. Helicobacter pylori is a human-specific bacterium causing persistent infections in the stomach associated with pathologies ranging from chronic gastritis, peptic ulceration to gastric cancer. Development and progress of these gastric disorders are determined by various bacterial factors. The bacteria express numerous well-known adhesins, vacuolating cytotoxin VacA, serine protease HtrA, urease, and four chromosomally encoded T4SSs. The pathology of H. pylori strongly depends on the T4SS encoded by the cag (cytotoxin-associated genes) pathogenicity island. This T4SS forms a needle-like pilus which is induced upon host cell contact, and its assembly is accomplished by multiple protein-protein interactions and various pilus-associated factors. The delivered substrates of the T4SS are the effector protein CagA and the LPS biosynthesis metabolite ADP-heptose. Various T4SS receptors have been described on the host cell, including integrins, CEACAMs, phosphatidylserine and cholesterol, suggesting that effector molecule delivery is a highly coordinated process. We demonstrate that H. pylori T4SS pilus formation during infection of polarized gastric epithelial cells occurs at basolateral membranes, and not at apical sites. Secreted HtrA paves the way for H. pylori by opening the cell-to-cell junctions through cleaving host cell junctional proteins such as E-cadherin, claudin-8 and occludin, followed by paracellular transmigration of the bacteria across the polarized cell monolayer. In this fashion, H. pylori travels to basolateral membranes and inject CagA. After delivery, CagA becomes phosphorylated by oncogenic tyrosine kinases of the Src and Abl families, and mimics a host cell factor for the activation or inactivation of some specific intracellular signalling pathways. Several CagA-dependent and CagA-independent signalling capabilities of the T4SS have been identified, which include the induction of membrane dynamics, actin-cytoskeletal rearrangements and changing cell polarity, as well as pro-inflammatory, cell cycle-related and anti-apoptotic transcriptional responses. The contribution of these signalling pathways to pathogenesis during H. pylori infections is discussed.

Ursula Lavery, 
Technical and R&D Director Europe

Ursula joined Moy Park in 1987 as a Marketing Executive having graduated from Queen’s University, Belfast with a BSc (Hons) in Food Science. Ursula moved into Technical and Quality Management and since then has steadily help build Moy Park’s reputation as a leading food company with absolute commitment to food safety and quality. Appointed to the Executive Board as Technical Director Europe in 2013, now Technical and R&D Director Europe, Ursula is responsible for establishing an Integrated Europe-wide Technical organisation. Recognised as a leading authority on Food Safety, Ursula has been involved in several advisory bodies including the FSA Acting on Campylobacter Together (ACT) board, IGD Technical Leadership Forum, Chilled Food Association (CFA) Executive Committee, and is a board member of the Northern Ireland Food and Drink Association (NIFDA) and the Industrial Advisory Board of the Institute for Global Food Security at Queen’s University Belfast.

Ursula is also a non executive board member of Centre for Innovation and Excellence in Livestock (CIEL).

Campylobacter - management in a commerical context?
Campylobacter – management in a commercial context?

Moy Park produces up to 6 million chickens a week, supplying own label products into leading retailers and foodservice providers throughout the UK, Ireland and Europe. This keynote presentation will outline Moy Park’s Campylobacter journey to date and gives an industry perspective on Campylobacter within the UK chicken supply chain and our work with academic partners.
Following the first publication of a Campylobacter retail survey by the UK Foods Standard Agency (FSA) in 2014 there has been major media and public focus on the subject. However, Moy Park has been working on Campylobacter control strategies for over 15 years. Millions of pounds have been invested and continue to be invested in research and development projects in conjunction with leading academics to continue to drive Campylobacter reduction. This presentation summarises the work we have undertaken with our partner farmers, processing facilities and academic partners, which highlights the leading role industry has taken in the absence of applied scientific solutions to tackle this issue.

Richard L. Guerrant, M.D.,
Founding Director, Center for Global Health

Dr. Guerrant is the Thomas H. Hunter Professor of International Medicine in the Division of Infectious Diseases and International Medicine at University of Virginia, and is Founding Director of the Center for Global Health at UVa, one of the first Trans-University Centers for Global Health.  He is a member of the IOM/National Academy of Medicine and formerly chaired its Board on Global Health. Having lived and worked in Congo, Bangladesh and Brazil and trained at Davidson College, UVa, Harvard-BCH and Hopkins, his research is focused on understanding and ameliorating the long-term impact of diarrhea and repeated enteric infections in developing countries. In his longstanding collaboration with the Federal University of Ceará in Northeast, Brazil he has conducted NIH-funded field research on interventions for childhood diarrhea for more than 25 years (5 U01 AI026512), in which he, among others have discovered the vicious cycle of diarrhea or enteric infections and malnutrition with ablation of catch up growth by increasing diarrhea burdens and long-term consequences for stunted growth and cognitive development.

He further discovered that the cognitive deficit most affected was Alzheimer-like semantic fluency impairment and hence examined the ApoE4 allele and found the initially surprising protection against diarrhea and its cognitive impairment in children with heavy diarrhea burdens, perhaps helping explain the evolution of this troubling allele.  He is senior editor of 7 books including “Tropical Infectious Diseases,” “At the Edge of Development: Health Crises in a Transitional Society,” and is author of over 650 scientific articles (18 with UVa’s 3 Nobel Laureates, Gilman, Murad and Marshall) and reviews, and has just published his book on “Evolution of Evolution: The Survival Value of Caring.” He is past president of the ASTMH and recipient of its highest honor, the Walter Reed Medal; as well as the IDSA Mentor Award; Virginia Outstanding Scientist; UVa’s highest honor, the Thomas Jefferson Award, and the NFID Maxwell Finland Award.

Guerrant loves kayaking with his high school sweetheart and wife of 53y and boating with kids and grandkids.

From Vibrio Obscurity to Major Health Morbidities: Lessons from ‘C. fetus,’ jejuni, ‘pylori’ & hyointestinalis
“From Vibrio Obscurity to Major Health Morbidities: Lessons from ‘C. fetus,’ jejuni, ‘pylori’ & hyointestinalis” Richard L. Guerrant, MD; University of Virginia, Charlottesville
After an overview of early pioneers, Guerrant will review its initial detection only in otherwise sterile blood cultures (including his own 1978 review of 5 patients and all 91 reported cases, with early virulence trait testing, including enterotoxin, LT, ST, invasiveness, serum sensitivity & cytotoxin [Am J Med 65: 584, 1978]); Jean Paul Butzler’s prescient expansion of our “lamp-post” using filtration and temperature to include detection in fecal specimens [J Peds 82: 492, 1973]; Skirrow’s selective media for this ‘new disease,’ early studies of field culture conditions, cytotoxin/s and serum sensitivity; through 10 years and little known Barry Marshall stories from the 10 years he was working in Dick’s lab in the mid-1980s – including studies showing common achlorhydria in Brazil and the clear reason it could withstand its gastric acid niche [Gastroenterol 99: 697, 1990] to his latest work developing murine models of Campylobacter diarrhea and enteropathy [PLOS Pathog 14: e1007083, 2018; and unpublished], and their use in assessing potential interventions.

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