Menzies Foundation interview

I was interviewed recently by the Menzies Foundation, of whom I am the 2005 alumni. Here is the Q&A.

What is your job?

Professor of Microbiology & Immunology at the University of Leuven (Belgium) and Director of Translational Immunology in the Flemish Biotechnology Institute.

What is the most fulfilling aspect of your work?

Discovery. Science is really a terrible career in so many ways, and yet it attracts many of the best and brightest because it holds out the promise of discovery. There is nothing quite so satisfying as unravelling a new gene network that leads to diabetes, or finding the mutation that holds the key to curing a sick child.

What is the book that has influenced you the most?

Bad Pharma by Ben Goldacre should be a must-read for anyone in the medical research industry. It is a book that is shocking in how it reveals systemic defects in pharmaceutical research, development and sales, and yet it is also eminently practical (even hopeful) in giving simple advice that would remedy the situation.

Who would you most like to meet and why?

Sir David Attenborough. A gentleman in the literal sense of the world, since childhood Sir David has nurtured in me (and countless others) a love of biology. For me, Sir David is the world’s most effective advocate for animal rights, environmentalism, evolution and atheism. All this is perhaps because he rarely talks about any of these topics directly; he cultivates the fertile mind and plants the seeds of knowledge.

What are your passions outside of work?

As Rosalind Franklin said, “Science and everyday life cannot and should not be separated”.

How do you describe leadership?

Leadership is moving forward in a way that inspires others to move forward with you. A scientific leader will open up a new field of research, opening the gates for others to follow and build upon. The best scientific leaders are those allow others to take the lead in building once the new field is open and look instead for the next opportunity for breakthrough.

Who would make a better leader? Engineer, doctor, researcher or lawyer and why?

The effectiveness of a leader will always depend on the context, and the individual’s qualities will always trump that of professional training. That said, different professions do hone different skills. Engineers apply proven rules with precision, doctors are trained at pattern recognition and decision making, and lawyers are trained to find loopholes to prosecute their agenda.  As a researcher myself, I would say our most important attribute is the ability to critically assess our own opinion based on data available, and, most importantly, change our opinion if new data does not support it. Perhaps over the short-term the training given to engineers, doctors or lawyers may be the most efficient, but for long-term progress, nothing beats the scientific approach of data over ideology.

If you were Prime Minister of Australia, what would you do first?

Looking at the bigger picture, the most important change needed is to bring the scientific approach into policy creation and political decision making. By this I mean an approach to policy where we start by critically looking at all the data (and not just the data that supports our ideology), assessing the effectiveness of previous policy approaches (with an international eye), designing new policy (that include measurements of effectiveness), and tweaking policy when failures are identified. This scientific approach to policy should be standard, but many of the failures of the current government stem from a triumph of ideology over data. Australia’s terrible record on the environment (such as our failure of leadership on climate change) stems from a failure to accept the consensus data on the scale of the problem. Our record on refugee rights is not only a moral failure, it is also a data failure – a key policy of the government is to keep data on the abysmal conditions of refugees away from the voting public. Opponents of same-sex marriage prophesize varied doomsday scenarios without looking at the decade-long experiences in Europe. Economic policies seem more tailored to the electoral cycle than to long-term objectives, and so forth.    

Graduation of Dr Anh Nuygen

Congratulations to Dr Anh Nuygen, who graduated with her PhD from our lab!

Anxiety increases the risk of gastrointestinal infection and long-term complications

A study in the aftermath of 2010 tap water contamination in the Belgian towns of Schelle and Hemiksem provides valuable insights into the cause of irritable bowel syndrome. A team comprised of scientists at VIB and KU Leuven has made significant progress in uncovering the connection between psychological factors and the immune system. Their findings are based on an investigation of a massive drinking water contamination incident in Schelle and Hemiksem in 2010, and are now published in the leading international medical journal Gut.

In December 2010, the Belgian communities of Schelle and Hemiksem in the province of Antwerp faced an outbreak of gastroenteritis, with more than 18,000 people exposed to contaminated drinking water. During the outbreak, VIB and KU Leuven set up a scientific task force to study the incident’s long-term effects, led by Guy Boeckxstaens and Adrian Liston.

Seizing an unexpected opportunity

Adrian Liston: “The water contamination in Schelle and Hemiksem was an ‘accidental experiment’ on a scale rarely possible in medical research. By following the patients from the initial contamination to a year after the outbreak we were able to find out what factors altered the risk of long-term complications.”

Anxiety and depression affect immune system

The scientists found that individual with higher levels of anxiety or depression prior to the water contamination developed gastrointestinal infections of increased severity. The same individuals also had an increased risk of developing the long-term complication of irritable bowel syndrome, with intermittent abdominal cramps, diarrhea or constipation a year after the initial contamination.

Guy Boeckxstaens: “Irritable Bowel Syndrome is a condition of chronic abdominal pain and altered bowel movements. This is a common condition with large socio-economic costs, yet there is so much that still remains to be discovered about the causes. Our investigation found that that anxiety or depression alters the immune response towards a gastrointestinal infection, which can result in more severe symptoms and the development of chronic irritable bowel syndrome.”

Psychological factors key in preventing long-term complications

The study’s results provide valuable new insight into the cause of irritable bowel syndrome, and underscore the connection between psychological factors and the immune system.

Adrian Liston: “These results once again emphasize the importance of mental health care and social support services. We need to understand that health, society and economics are not independent, and ignoring depression and anxiety results in higher long-term medical costs.”

For more details, see the original publication: Wouters*, Van Wanrooy*, Nguyen*, Dooley, Aguilera-Lizarraga, Van Brabant, Garcia-Perez, Van Oudenhove, Van Ranst, Verhaegen, Liston*, Boeckxstaens*. * shared authorship. Psychological comorbidity increases the risk for postinfectious IBS partly by enhanced susceptibility to develop infectious gastroenteritis. Gut. 2015, in press. 

Update on Wednesday, July 8, 2015 at 7:33PM by Adrian Liston

An article written in Healio on our study

New diabetes drug-screening model available

Lab name change

We are changing out name from the Autoimmune Genetics Laboratory to the Translational Immunology Laboratory. This new name better reflects our research interests, which have moved broader than just autoimmunity and have also taken on a strong translational angle.

Within the Translational Immunology laboratory we will have two major research divisions: Discovery Immunology and Applied Immunology. Discovery Immunology will focus on unravelling more of the basic biology of the immune system, with an emphasis on regulatory T cells and the process of diabetes. Appled Immunology will focus on the human immune system, containing our immune phenotyping platform and gene discovery program. Advances in each division are expected to feed into each other.

VIB immune phenotyping platform open for industry collaboration

Neurodegenerative mouse strain discovered

Sometimes science works by chance.

In a mouse colony that we were breeding to study myeloproliferative disease, just by chance we had a few mice that just started shaking. Seizing the chance to study these further, we found out that our colony had generated a spontaneous mutation in the gene Mbp, a structural component of the insulating layer that keeps nerves insulated (in the same way that the plastic coating of metal wires is required for electricity cables). Without insulation of their nerves, the mice developed an erratic shaking and later on developed seizures. This work ended up revealing new aspects of the regulation of nerve insulation genes, and has been published in the journal Brain Research.

Read more: Staats, Pombal, Schönefeldt, Van Helleputte, Maurin, Dresselaers, Govaerts, Himmelreich, Van Leuven, Van Den Bosch, Dooley J, Humblet-Baron*, Liston*.Transcriptional upregulation of myelin components in spontaneous myelin basic protein-deficient mice. Brain Res. 2015 in press.

New cause for early-onset lupus discovered

In a new study out by the Autoimmune Genetics Laboratory, we have discovered a new genetic cause for early-onset systemic lupus erythematosus - mutation in the gene IFIH1. In 2014, mutations of this gene were independently found to cause the neurodegenerative disease Aicardi-Goutières syndrome (AGS). Despite lupus and AGS manifesting as clinically different symptoms, this study shows that mutation in the same gene causes both diseases. The mutation in IFIH1 works via driving excessive production of the cytokine IFN alpha, so this discovery opens up the possibility for treatment once anti-IFN alpha antibodies (currently in development) are approved for use. 

Read more: Van Eyck, De Somer, Pombal, Bornschein, Frans, Humblet-Baron, Moens, de Zegher, Bossuyt, Wouters* & Liston*. IFIH1 mutation causes systemic lupus erythematosus with selective IgA-deficiency. Arthritis Rheumatol. 2015, in press.

If you would like to support our clinical research, and allow us to take on more cases like this one, you can make a tax-deductable donation the Ped IMID fund, by transferring to IBAN-number BE45 7340 1941 7789, BIC-code: KREDBEBB with the label "voor EBD-FOPIIA-O2010".

New fund to support translational research into paediatric inflammatory diseases

A new fund has been set up to drive bench-to-bedside research for children with inflammatory immune diseases. The Ped IMID fund (Fonds Pediatrische Immuun-inflammatoire Aandoeningen) was set up by Prof Carine Wouters (Pediatric Rheumatology), Prof Patrick Matthys (Immunobiology) and Prof Adrian Liston (Autoimmune Genetics) to build on our strong research cooperation. More than merely "translational research", where basic science is pushed into the clinic, our group performs "dialog research", where we meet regularly to discuss the clinic and the science of the most difficult-to-treat patients. We use the clinic to inform the research and the research to inform the clinic, and have already had multiple break-throughs in understanding and treating children with rare inflammatory diseases. 

If you would like to support our research, and allow us to take on more cases, you can transfer a tax-deductable donation to IBAN-number BE45 7340 1941 7789, BIC-code: KREDBEBB with the label "voor EBD-FOPIIA-O2010".

New disease (and cure!) found

As part of an ERC funded research program, the Autoimmune Genetics Laboratory is searching the genomes of young children with severe immune diseases to look for novel genes (and hopefully treatments). In a collaboration with Prof Carine Wouters and Prof Isabelle Meyts at UZ Leuven, we found mutations in a new gene, CECR1, in three severely ill children. Two of the children were born with a severe immune deficiency, making them prone to infections, while the third developed an inflammatory disease known as Castleman's disease. Mutations in the same gene, which produces the protein ADA2, were independently found by two other groups to give vascular disease and early-onset stroke. 

These studies identify ADA2-deficiency as a previously undiagnosed primary immunodeficiency which includes components of immune deficiency, inflammation and vasculopathy. Most importantly, this new diagnosis comes with a successful cure: prior to genetic diagnosis, our clinical collaborators were able to successfully treat the disease with bone-marrow transplanation (for the immunodeficient patient) or tocilizumab (for the Castleman's disease patient). These results therefore not only add to our knowledge about medical genetics, but also provide a direct diagnosis-treatment pathway for any new children identified with these severe diseases.

Read more:

Van Eyck, Hershfield, Pombal, Kelly, Ganson, Moens, Frans, Schaballie, De Hertogh, Dooley, Bossuyt, Wouters, Liston* and Meyts*. Hematopoietic stem cell transplantation rescues the immunologic phenotype and prevents vasculopathy in patients with adenosine deaminase 2 deficiency. J Allergy Clin Immunol. 2015 Jan;135(1):283-287.e5.

Van Eyck, Liston and Wouters. Mutant ADA2 in vasculopathies. N Engl J Med. 2014 Jul 31;371(5):480

Van Eyck, Liston and Meyts. Mutant ADA2 in vasculopathies. N Engl J Med.  2014 Jul 31;371(5):478-9.

If you would like to support our clinical research, and allow us to take on more cases like this one, you can make a tax-deductable donation the Ped IMID fund, by transferring to IBAN-number BE45 7340 1941 7789, BIC-code: KREDBEBB with the label "voor EBD-FOPIIA-O2010".