Neutrophils, which are the main immune cells in the body, cause inflammation by destroying an anti-inflammatory molecule known as PGRN, researchers at the Max-Planck-Institute of Neurobiology, Germany, have found.
Neutrophils are the first cells of the immune system to respond to invading microorganisms by internalising and destroying them using proteins known as neutrophil serine proteases (NSPs).
While neutrophils are considered the "good guys" in such circumstances, they also contribute to the noninfectious chronic inflammation that underlies various diseases, including autoimmune diseases such as rheumatoid arthritis.
However, it is still not known what role does NSPs play in noninfectious chronic inflammation.
The scientists used mice lacking two very similar NSPs, PR3 and NE, and showed that these two NSPs have a crucial role in one form of noninfectious chronic inflammation.
After a close analysis it was found that PR3 and NE destroy an anti-inflammatory molecule known as PGRN and in this way help to promote inflammation in the absence of invading microorganisms.
This led the authors to suggest that these data provide rationale for considering inhibitors of NSPs as anti-inflammatory drugs.