Dr George Bou-Gharios
Dr George Bou-Gharios is a reader in matrix biology, renal medicine, Imperial College London, and the holder of two Arthritis Research UK project grants.
What does your work involve?
My time is divided between research, teaching and administration. I'm head of the Infection & Immunity Research group at Glasgow Dental School and teach biomolecular sciences to undergraduate dental students and on MSc courses. I've had a longstanding interest in the development of improved molecular diagnostic tests for identifying microorganisms in clinical specimens. I'm particularly interested in the role of oral bacteria in systemic infections. A major area of my research lies in identifying the bacteria associated with biofilms on the surface of infected prosthetic hip joints using both culture-dependent and culture-independent methods in a study currently funded by Arthritis Research UK. I've recently applied this approach in investigating the microbial basis of various forms of canine arthritis.
How long has Arthritis Research UK been funding you?
I've been funded on and off since 1997. There's an art to writing grant proposals. Since English isn't my mother tongue it's twice as hard for me to convey the message.
What’s the most important thing you have found out in the past 12 months? Why?
Osteoarthritis develops as a result of the degrading power of enzymes in the joints. We tried to block these enzymes that erode the joints by using natural inhibitors against the enzymes. It's not a straightforward story because we found out that some of these enzymes are crucial for maintaining healthy joints. The devil is in the detail, as in humans there are 23 members in the largest enzyme family alone and the process of elimination has just began. By creating an inhibitor that could avoid the useful enzymes, we'd be able to treat osteoarthritis without affecting the maintenance of the joints.
What do you hope or expect to achieve as a result of your Arthritis Research UK funding?
I hope that what I do will establish a clearer understanding of how, in arthritis, cells that are embedded in the ‘matrix’ (which they secrete) respond to outside signals. By understanding the cross-talk, we'd be able to devise strategies which would halt the progression of the disease.
What do you do in a typical day?
My day begins with an hour-and-a-half train journey to work where I do most of my scientific reading! Once at the office, a double espresso is a great stimulus and sets the ball rolling before meeting one of my team members to discuss their research. Lunch is a sandwich over a computer screen, reading and answering emails. Some of our college committee business is conducted mainly in cyberspace. The afternoon is a time for writing papers and grant proposals, which are refined on the journey back home.
What's your greatest research achievement?
I think the greatest is yet to come! But thus far discovering the DNA segment that's important in regulating the most abundant protein (collagen type I) found in mammals is a good start.
Why did you choose to do this work?
I've always been fascinated with matrix molecules and their multi-tasking. They form the scaffold which shapes our organs, signal to cells and are essential for repair. Did you know that collagen type I is strong enough in bundles to support the Empire State Building? The balance between making and the removal of these molecules in the body is tightly controlled. I'm intrigued by how our bodies maintain such a balance and how this is impaired in diseases such as fibrosis or osteoarthritis: two faces of the same coin!
Do you ever think about how your work can help people with arthritis?
Every day. When I started my PhD some years ago, I was funded by a small charity called the Mucopolysaccharidosis Society. Occasionally, through them, I'd meet the children who were affected by these diseases. I've never forgotten the distress I felt following these encounters. Thus, the ultimate aim of relieving the suffering in arthritis has permeated my work. I'm also mindful of all the caring people who've raised the money to pay for this research. We spend this money wisely with the hope that what we do may benefit the sufferers in the near future.
What would you do if you weren’t a scientist?
I'd be a journalist or a playwright.
I'm married with two kids and live in Buckinghamshire. I enjoy the theatre and would buy any electronic gadget if I could afford it.
This article first appeared in Arthritis Today Spring 2008, issue 140.