U-M team shows cells' role in inflaming airways in mice, and finds similar cells in the blood of humans with asthma, pointing to a possible target for treatment
ANN ARBOR, Mich., May 7, 2012 /PRNewswire-USNewswire/ -- For most people with asthma, a couple of puffs from an inhaler filled with steroids makes breathing easy. But if their lungs become resistant to the calming effect of that medicine, they live in fear of severe asthma attacks that could send them to the hospital – or worse.
Now, new research from the University of Michigan Health System may help explain what's going on in the lungs of these steroid-resistant individuals. The findings could aid the development of new treatment options, and of better ways to identify people at risk of becoming steroid-resistant.
The U-M scientists have discovered a new type of cell in mice that appears to be crucial to causing asthma symptoms -- even in the presence of steroid. The research, published in Nature Medicine, also showed that people with asthma have a very similar cell type in their blood at higher levels than people without the condition.The researchers call the new cell type T2M, for type 2 myeloid – reflecting its origin in the bone marrow and its involvement in the "type 2" immune response that causes asthma symptoms. In the lungs, T2M cells were shown to receive specific distress signals sent out by cells in the lung lining – and to produce molecules that lead to more inflammation. The role of these cells was uncovered after a persistent search by a team led by pathology professor Nicholas Lukacs, Ph.D., and Bryan Petersen, a student in U-M Medical School's Medical Scientist Training Program who recently completed a Ph.D. thesis based on these findings. They found the cells while examining the role of a signaling molecule called interleukin 25, or IL-25 -- a type of protein called a cytokine that other asthma-probing scientists and pharmaceutical companies are also looking closely at.