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".

PhD graduation

Congratulations to Dina Danso-Abeam who just graduated from her PhD in the laboratory!

Lab retreat

Great science at a very successful annual lab retreat! Special thanks to Michelle Linterman, Sylvie Lesage and An Goris as external evaluators, and our own Wim Cockx for flawless planning.