Your first research in that area?

First, I worked on a mouse model of post-infectious IBS triggered by a parasite, Trichinella spiralis. In some genetically predisposed mice, this parasitic infection induces a longterm gut dysfunction The mice initially develop diarrhea, to expel the parasite from the gut which then converts into slow intestinal transit accompanied by increased pain perception such as caused by bowel distension Interestingly exposing the previously infected mice to antigens from T spiralis stimulates the immune system and maintains the gut dysfunctionHowever my first project involving bacteria was to develop a mouse model of functional dyspepsia using chronic infection with Helicobacter pylori We demonstrated that mice which had been infected with H pylori over three months had delayed gastric emptying as well as altered perception of the stomach distension As you can see I started on several fronts but these studies gave me my very first insights into the interplay of immune system and microbiota that can result in altered bowel function

Premysl Bercik is a Professor of Gastroenterology at the

Department of Medicine at McMaster University, Hamilton,

Ontario, Canada, and member of the Farncombe Family Digestive

Health Research Institute. He received the international

grant in 2020 for his work on “Gut microbiota and post

antibiotics disorders”.

The first time you made the link between microbiota and IBS (Irritable Bowel Syndrome)?

After finishing my medical studies in the Czech Republic, I had the opportunity to join the University of Lausanne, in Switzerland, where I studied the function of the enteric nervous system and gastrointestinal peristalsis. Back then, we hardly knew anything about the gut microbiota and its role in IBS. A presentation by my current mentor, Stephen Collins, spurred my desire to continue my postdoctoral studies at McMaster University in Canada: he spoke about the pioneering notion that even very low levels of pro-inflammatory cytokines could alter gastrointestinal function. Now, three decades later, it is well established that low-grade inflammation is a key mechanism in IBS, however it took us long time to realize that the microbiome is the driver of this intestinal inflammation.

Professor Bercik’s

firsts

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