esis continues throughout life, the researchers found. Through a still undiscovered signal, the microbe apparently induces the intestinal cells to make one of its favorite foods. The bacterium even has a fucose sensor that informs it when this food source is scarce, according to Gordon and his colleagues.
The capacity of B. thetaiotaomicron to instruct intestinal cells to make fucose was just a hint of things to come. To get a more comprehensive picture of the bacterium's influence, Gordon's group turned to microchip-size devices, called DNA microarrays, that monitor the activity of thousands of genes at once (SN: 3/8/97, p. 144).
With such instruments, the scientists took a snapshot of the gene activity in the mouse intestine. By comparing tissue from germfree mice and mice hosting B. thetaiotaomicron, the team found that the presence of the bacterium significantly reduces or boosts the activity of about 100 of the approximately 25,000 rodent genes in the microarray survey.
Some of the intestinal genes triggered by the microbe help mammals absorb and metabolize sugars and fats, Gordon and his colleagues reported in 2001. Other activated genes fortify the cellular barrier that prevents bacteria, both dangerous and friendly, from sneaking out of the intestine into other tissues and the bloodstream. And yet other affected genes determine how the intestine detoxifies compounds and how the gut matures.
"We were amazed at the breadth of normal intestinal functions affected by a single microbe," says study coauthor Lora V. Hopper. Gordon adds, "It's difficult to anticipate the full range of host functions that might be manipulated by these microbes."
The genetic activity that the researchers didn't see in the bacteria-colonized mice was interesting, too. Even though the originally germfree mice had never encountered B. thetaiotaomicron before, there was no increase in activity of the genes underlying an immune or inflammatory response. That's a reflection of the microbe's still mysterious skill at convincing a host that it's a friendly visitor and not a danger, says Gordon.
Among the intestinal genes activated by B. thetaiotaomicron is one suspected to stimulate the growth of new blood vessels. The finding spurred Gordon's group to investigate the microbe's control over the system of blood vessels that runs through the GI tract. These blood vessels are crucial to a body's absorption of nutrients.
The researchers discovered that their germfree mice have a poorly formed network of the capillaries that normally supply the inner intestinal surface with its blood supply. This could partly explain the difficulty that germfree animals have absorbing nutrients.
The team also found that it could stimulate germfree mice to grow a normal network of intestinal capillaries by exposing the animals to either a full complement of microflora or just B. thetaiotaomicron. The investigators reported the finding in the Nov. 26, 2002 Proceedings of the National Academy of Sciences.
This is a vivid illustration that the physical development of the gut can depend on the microbes that normally inhabit animals, says Gordon. The researchers also found cells in the mouse gut that seems to work with the microbes to spur vessel growth.
In the small intestine, so-called Paneth cells normally secrete antimicrobial compounds (SN: 8/26/00, p. 135: Available to subscribers at http://www.sciencenews.org/20000826/fob8.asp). This keeps the intestine healthy by protecting other cells that continually replenish the gut lining. Gordon's team created germfree versions of mutant mice that lack Paneth cells and found that B. thetaiotaomicron couldn't trigger the maturation of blood vessels in such rodents. While most investigators have regarded Paneth cells simply as defenders against invading bacteria, it makes sense that these cells mediate interactions between a host and its natural microflora, says Gordon. "What better cell to respond to the presence or absence of a microbe?" he remarks.
The Paneth cell is at the heart of another microbe-intestine interaction uncove