Scientists Identify a Way to Turn Off Asthma Attacks
A new study revealed that the regulatory proteins that control the inflammatory immune signaling pathways in cells responsible lung-constricting asthma attacks can be turned off.
The study, published in the Journal of Biological Chemistry, showed that the overabundance of one type of immune cells called M2 macrophages in the lungs is somewhat responsible for asthma attacks. The researchers noted that turning off the signaling pathway that activates the M2 cells could prevent allergic attacks.
"Asthma patients are constantly firing through this pathway because those proteins are stuck in the 'on' position, without proper control by other proteins that shut down this reaction," explained Nicola Heller, Ph.D., assistant professor of anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine, in a press release.
For the study, the researchers investigated the role of two proteins, GRB10 and p70S6K, in the control of the IRS-2 pathway. IRS-2 is a protein where the immune system chemical interleukin 4 (IL-4) passes through to activate the M2 cells. The researchers analyzed the chemical changes of the IRS-2 protein in immortalized cultures of human white blood cells.
The researchers found that the IRS-2 protein appeared in two different forms. In its first form, or "on", the protein allows the IL-4 to pass through. On the other hand, the "off" form of the IRS-2 protein stops the IL-4 from activating the cells into M2 macrophages.
In their experiments, the researchers discovered that decreased in the activity of GRB10 and p70S6K proteins resulted in more of the "on" form of the IRS-2, suggesting that the two proteins is responsible for turning off IRS-2 and decreasing M2 production.
The results of the experiments on how to control the M2 macrophages production could also be a great help in the field of cancer and other disorders, such as obesity. M2 macrophages cells are known to play a regulatory role in tumor growth and fat deposition.