A new study, published in Science, explores what happens in the body when bacteria like Yersinia and Salmonella are at peak activity. That could come in handy. Not only because Yersinia still exists and because antibiotic resistance is a growing problem, but because the new knowledge can be transferred to help understand other diseases.
It turns out that immune cells are so dedicated at their jobs that they explode themselves to release proteins that fight the invading bacteria and resulting damage. The explosion does not go unnoticed and warns the other immune cells. The immune cells sacrifice themselves to let the other cells know what is going on.
The process is so explosive that it is called pyroptosis.
What happens is that the immune cell forms small pores on its surface. This causes water to flow into the cell, which then swells until it bursts. When the cell explodes, it also releases substances that inhibit the invading bacteria from growing and that alert the other cells. Pretty effective, right?
Immune system backup kicks in
Sneaky Yersinia knows all this, and tries to camouflage itself and secretes an antidote. The NTNU researchers figured out that the body knows that Yersinia disguises itself. At this point, the action starts to get really involved, but the article in Science explains that the immune cells initiate a backup mechanism that is triggered in a way not previously understood.
“These findings show us complicated mechanisms that occur in the immune system to counter infection, but they may also apply to other diseases. Some of the same phenomena can happen in diseases that cause inflammation in the body in general, such as food poisoning or Alzheimer’s disease. So these findings can also increase our understanding of inflammation, which happens in most diseases as changes occur in the body,” says Lien.
This article has been republished from materials provided by the Norwegian University of Science and Technology. Note: material may have been edited for length and content.
Orning, P., Weng, D., Starheim, K., Ratner, D., Best, Z., Lee, B., . . . Lien, E. (2018). Pathogen blockade of TAK1 triggers caspase-8–dependent cleavage of gasdermin D and cell death. Science, 362(6418), 1064-1069. doi:10.1126/science.aau2818