Inflammation is a standard part of our bodies' immune system response. But sometimes this response becomes hyperactivated in our lungs, causing inflammation to continue unchecked, which can be fatal. Many deaths from COVID-19 have been due to excessive inflammation, which results in acute lung injury.
A group of researchers at the University of Illinois Chicago have investigated how lungs counterbalance inflammation. Their work points to cells in the lung that reduce inflammation by removing cellular debris, ingesting harmful bacteria and releasing anti-inflammatory proteins. What's more, these cells can be trained by an initial infection to do this job even better during a subsequent infection.
The researchers found that after an initial exposure to a bacterial toxin, lung immune cells called alveolar macrophages helped reduce the severity of inflammation brought on by a second exposure to the bacterial toxin one week later. The benefit of this "memory" or "training" was present even when the second exposure occurred a month later, explained senior author Dr.
Clearing out this debris is important because its persistence can trigger the immune system to continue to react, thus increasing inflammation." Because this debris isn't specific to one type of infection, these trained macrophages might help reduce the risk of acute lung injury from subsequent infections that arise from a different disease. The researchers found that the molecules involved in the removal of cell debris were higher in the trained alveolar macrophages.
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