Bacteria that cause dental disease hijack the bloodstream to travel to the colon where they latch on to tumours and help them grow, new research shows.
Biologists from the US and Israel discovered that the common Fusobacterium nucleatum bacteria uses a protein called Fap2 to stick to colorectal cancer cells and shields the tumour from the body’s immune system.
The work, published in Cell Host & Microbe, may not only give oncologists a means to block colorectal tumour growth, but also a means to deliver cancer-killing drugs.
Only in the past few years has the influence of microbes that dwell in and on our body on the growth and progression of colorectal cancer been unveiled.
One particular strain, F. nucleatum, emerged as an interesting example. Colon tumours tend to have lots of the rod-shaped bacteria stuck to them while the surrounding tissue is pretty much bare.
But the bacteria’s preferred habitat isn’t the gut – it’s the mouth, where it binds to other microbes to form blobs called biofilms. These masses of bacteria are the plaque that accrues on tooth enamel and along the gum line and can cause diseases.
So how does F. nucleatum make the journey from mouth to colon? The obvious answer is it’s swallowed and travels through the gastrointestinal tract, but studies searching for it in the stomach and small intestine have largely drawn a blank.
Jawad Abed and Johanna Emgard from the Hebrew University in Israel and colleagues thought the bacterium may hitch a ride in the bloodstream. To test this, they injected fusobacteria into the vein of mice with colorectal tumours.
They found it didn’t matter if the tumours were precancerous or malignant – fusobacteria in the blood sought them out and stuck on tight, but largely ignored the surrounding healthy tissue.
The colon of mice without tumours had no fusobacteria, suggesting that a tumour is required for the bacteria to make the jump from the bloodstream.
Using human and mouse cells, the team uncovered the sticking mechanism favoured by fusobacteria.
A protein hanging off the outside of the bacterial cell, Fap2, recognised and grabbed onto a sugar found on colorectal tumour cells called D-galactose-β(1-3)-N-acetyl-D-galactosamine (thankfully shortened to Gal-GalNac).
Previous work showed that Fap2 is instrumental in helping colorectal tumour cells fly under the immune system’s radar, dampening the actions of T-cells that would normally kill the cells, and allowing the tumour to grow and the bacteria flourish.
Gilad Bachrach, also from the Hebrew University and a senior author of the study, acknowledges that the work does have limitations. For instance, in some mouse models, colorectal tumours grow quickly – often within a few months. In humans, though, tumours tend to grow over years.
And will brushing teeth more often help keep the risk of colorectal cancer risk down?
Bachrach’s not sure yet: “Based on our findings, it’s too early to say whether we can prevent mouth bacteria from travelling through blood to the colon and promoting tumour formation or if some people are more at risk than others.”
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