To examine this possibility, Chow genetically altered the bacterium to inactivate its "secretion system." The secretion system is a collection of proteins the microbe uses to send chemical messages to its host; Mazmanian says it represents a biological "needle and syringe" that delivers bacterial molecules directly into eukaryotic cells. Although the specific functions and identities of these chemicals are unknown, they appear to establish a truce between the bug and the host's immune system.

When Chow genetically disrupted the secretion system-shutting off this communication-she saw two unexpected and intriguing effects. First, the size of the H. hepaticus population expanded dramatically, leading to dysbiosis. In turn, the host immune system ramped up its activity. This manifested in inflammation-the body's response to infection or injury.

"The bacteria appear to have struck a deal with their host," Mazmanian says. They keep their own numbers low so they don't overwhelm the immune system, and in return, the immune system leaves them alone. "The bacteria need the secretion system to put the host in 'don't attack' mode." In return, the presence of the bacteria does not induce inflammation, as would be the case with a pathogen that has not evolved a similar "agreement."

"There has to be communication. It could be peaceful-as is the case for symbionts-or it could be an argument-as is the case for pathogens. But when this molecular dialogue breaks down, it's probably harmful to both microbe and man," Mazmanian says.

Disrupt that communication, and the balance gets thrown out of whack. "Inflammation leads to cancer, and this bacterium has been associated with inflammation and colon cancer in animals," he says. Understanding if dysbiosis causes disease in humans could lead to therapies based on restoring the healthy microbial balance in the gut.

Source: California Institute of Technology