Here’s how the body prevents helpful bacteria from causing disease

The human body is home to millions of friendly bacteria but how does it distinguish helpful microbes from foreign invaders?

A new study on mice sheds light on how a body’s immune system develops mechanisms to allow the presence of good bacteria.

The degree to which the immune system tolerates a given bacterium depends on what the scientists call a “friend/foe” decision-making system.

To see how the mechanism worked, the team from the NYU School of Medicine exposed mice to a type of bacteria known as the Helicobacter hepaticus.

Certain bacteria, such as those from the Helicobacter family, are generally considered helpful but can cause disease when genetic or environmental factors alter the normal balance. These types of bacteria are known as pathobionts.

The researchers looked at two types of cells in the immune system – known as the T cells – which are responsible for controlling the immune response to the bacteria.

Their findings showed that the Helicobacter hepaticus bacteria caused the immune system to produce a type of cell known as T helper 17 cells (Th17), which triggered inflammation, which is the body’s natural reaction against infection.

The researchers believe that the immune system of mammals, such as humans and mice, evolved so that Th17 cells specific to pathobionts are paired with another set of T cells that shuts down those Th17 cells.

This, according to the researchers, enables the body to develop tolerance to certain bacterial strains.

Evidence suggests that defects in such cells may enable bacteria to drive common inflammatory bowel diseases (IBD) like Crohn’s and ulcerative colitis, the researchers said.

Lead study author Dr Dan Littman, of the NYU School of Medicine, said: “Our findings represent a significant step toward clarifying the mechanisms that help the body manage the risk of keeping potentially dangerous, but often useful, bacteria around.”

The scientists say the next step in the research would be to identify the bacterial species contributing to IBD in humans.

The study is published in the journal Nature.