For a long time, doctors believed that our lungs were completely sterile—free of bacteria, viruses, or any other microbes.
Today, science paints a very different picture. Our lungs are constantly exposed to tiny invaders: allergens, bacteria, and viruses we inhale, including influenza and even SARS-CoV-2, the virus responsible for COVID-19.
Most of the time, our immune system handles these intruders without much trouble. But when inflammation spirals out of control, the result can be serious, long-lasting lung diseases.
Researchers at the University of Illinois Chicago (UIC) have now discovered that a small but mighty protein, called IL-10, plays a key role in keeping our lungs healthy and preventing diseases like pulmonary fibrosis and bronchiolitis.
Their findings were recently published in the journal Immunity.
Every human body hosts trillions of tiny organisms, collectively known as the microbiome. In the gut, they help us digest food.
On our skin, they keep moisture balanced. And in the lungs, they interact with immune cells to maintain a delicate balance between defense and peace. As Dr. Kiwook Kim, assistant professor of pharmacology and regenerative medicine at UIC, explains, “Our immune system needs to be strong enough to fight off threats without triggering excessive inflammation.”
One group of immune cells in the lungs, called interstitial macrophages, are particularly important in this process. These cells not only clear away dead cells and unwanted microbes but also help calm down inflammation when it’s no longer useful. Until now, scientists weren’t sure exactly how they did it.
The UIC team found that interstitial macrophages produce IL-10, a protein that acts as a messenger, sending “anti-inflammatory” signals to other immune cells. In experiments with mice that lacked IL-10 signaling, the researchers observed uncontrolled lung inflammation, even without any apparent trigger.
Things got worse when certain bacteria were present. Without IL-10, bacteria like Delftia acidovorans and Rhodococcus erythropolis were able to spark severe inflammation. “It’s the perfect storm,” explained Dr. Teruyuki Sano, co-author of the study. “When the bacteria are there and IL-10 is missing, inflammation and lung disease are much more likely to occur.”
This discovery could have important implications for conditions such as pulmonary fibrosis, chronic obstructive pulmonary disease (COPD), and follicular bronchiolitis. By understanding how IL-10 works to keep lung inflammation in check, doctors may one day be able to better predict, prevent, and treat these diseases.
What this research makes clear is that health often depends on balance: the balance between our immune system and the microbes we live with, and the balance between fighting infection and keeping inflammation under control. And sometimes, the smallest proteins make the biggest difference.
Source: University of Illinois at Chicago.
