MacrophageWIKIMEDIA, NIAIDMacrophages detect and kill pathogens, but also recognize and repair damage to host tissues. How the cells determine which response is required, however, is somewhat of a mystery. Now, researchers at the University of Oxford studying the macrophage toll-like receptor 4 (TLR4), which interacts with both bacterial lipopolysaccharide (LPS) and host protein tenascin-C, show that the two molecules trigger different pathways and proteins in the macrophages that govern contrasting responses. The findings were published yesterday (August 30) in Science Signaling.
“This is a very interesting paper. It addresses a big overall question of how does the immune system distinguish between infection and non-infectious tissue damage,” said immunologist Cynthia Leifer of Cornell University College of Veterinary Medicine in Ithaca, New York, who was not involved in the study. “The overall conclusion is that, through one innate immune receptor, with two different ligands, you can trigger two different types of outcome.”
LPS, also known as endotoxin, is a molecule found in the outer membrane of many different types of bacteria. Through its interaction with TLR4, LPS induces a strong inflammatory reaction in humans. Tenascin-C, on the other hand, is a protein found in the extracellular matrices of various host tissues. “There is not very much of it ...
