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Scientists have long thought of the fluid-filled sacs around our lungs as mere protection from outside damage. Turns out, it also contains powerful virus-eating cells that reach the lungs during a flu infection.

Not to be confused with phages, which are viruses that infect bacteria, these cells are macrophages, immune cells produced in the body.

“The name macrophage means ‘big eater.’ “They collect bacteria, viruses, cancer cells and dying cells. In fact, anything that looks foreign, they pick it up and destroy it,” said UC Rivers, who led the discovery team. Side virologist Juliet Morrison said. “We were surprised to find them in the lungs because no one had seen it before, that these cells go to the lungs when there is an infection.”

A paper published in Proceedings of the National Academy of Sciences During influenza infection, macrophages leave the external cavity and enter the lungs where they reduce inflammation and reduce the level of disease.

“This study shows that it’s not just what happens in the lung that matters, but also what happens outside of the lung,” Morrison said. can have a huge impact on disease and health,” Morrison said.

There are three main cavities in the body: one around the heart, the abdominal cavity, and the pleural cavity around the lungs. “Because it contains fluid, it prevents the lung from collapsing. However, people haven’t thought much about it being a complete organ in itself. This research could change that perception,” Morrison said. ” said Morrison.

Initially, researchers set out to understand the general question of what types of cells are present in the lungs during a flu infection. They took existing data on lung-related genes from studies of mice that either died or survived the flu. They then mined the data using algorithms to predict the types of cells that change in the lungs during infection.

“We took the big data and broke down which potential immune cells were present in the lung tissue,” Morrison said. “

Then, using a laser-based technique, the team tracked macrophages moving into the mice’s lungs, and observed what happened if they took those cells out of the equation. “When you take them out of the mouse, you see more disease and more lung inflammation,” Morrison said.

Morrison says she hopes the study will inspire other scientists to re-examine data sets from older studies. “Our approach was to take existing information and put it to new uses, and we were able to see something new,” he said.

Moving forward, the research team hopes to determine which proteins “tell” macrophages to migrate to the lungs. Once the protein signals are identified, it may be possible to develop drugs that increase either the number of macrophages, or their activity.

Strategies to boost human defenses against infection, rather than developing yet another antiviral, could offer people a flu treatment that will be more effective for longer. Morrison became interested in host therapy because resistance to antibiotics and antiviral drugs is a growing problem.

This problem occurs when germs such as bacteria and fungi develop the ability to defeat drugs designed to kill them. Misuse and overuse of medications is exacerbating the problem. According to the Centers for Disease Control and Prevention, more than 2.8 million drug-resistant infections occur in the United States each year, and more than 35,000 people die as a result.

“If we can increase what resolves the infection in us, we probably have a better shot. We’re less likely to develop resistance. The immune system is very complex, but it’s our best bet that we have Work with what’s there instead of chasing viruses that continue to elude our treatments,” Morrison said.

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