2 min readImmune Cells Sacrifice Themselves to Protect Us from Invading Bacteria
Trondheim, Norway — The stomach flu can turn the strongest individual into a limp dishrag. Snot and slime are going wild in kindergartens. This year’s flu is approaching in full swing.
You can have your fever-lowering drugs ready, but the flu is a strange thing. The same bacteria and viruses don’t hit everyone with the same intensity.
Some people get really sick, others less so. Some folks don’t get sick at all.
Why? What’s really going on in the body when viruses and bacteria sneak in the back door and gear up for a full-on party?
Black Death as a lifelong partner
A lot of researchers are intrigued by that very question. One of them is Professor Egil Lien at the Norwegian University of Science and Technology’s (NTNU) Centre of Molecular Inflammation Research (CEMIR). He splits his time between Norway and the the University of Massachusetts in the United States and is one of Norway’s foremost experts on how bacteria attack people.
Lien hasn’t chosen the easiest bacteria to get to know. He has opted to focus his study on a really nasty one called Yersinia pestis, known as the culprit behind the Black Death outbreak. Yes, the bacteria that killed a third of Europe’s population in the 1300s.
Lien has singled out precisely this bacterium as a lifelong research partner because it is a very deceptive one. Yersinia manipulates the immune system to hide from it, almost like a chameleon that changes color. It also kills cells that the body uses in the immune system.
For more effective medication
Now Lien, PhD candidate Pontus Ørning and other research colleagues have made a new discovery about what happens in the body when bacteria like Yersinia and Salmonella are at peak activity.
This information 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.
This knowledge can also be used to make more effective medicines. Their finding has been published in the November 30 issue of Science magazine.
Sacrifice themselves in warning
It turns out that immune cells are so dedicated to their jobs that they explode themselves to release proteins that fight 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.
Article adapted from a Norwegian University of Science and Technology news release.
Publication: Pathogen blockade of TAK1 triggers caspase-8–dependent cleavage of gasdermin D and cell death. Orning, P et al. Science (November 30, 2018): Click here to view.