In asthma, substances such as allergens irritate the airways and cause the smooth muscle cells around them to contract. With repeated attacks, lung tissues become damaged from cycles of inflammation and repair. Scar tissue forms, which forces the airways to change their shape, or remodel. The airway walls become abnormally thick, potentially interfering with breathing. Figuring out how to stop the thickening is a common goal among asthma experts. Now, Harvard School of Public Health Assistant Professor Daniel Tschumperlin and his colleagues have suggested a possible additional explanation for why the airways thicken, providing another research target. The work required the expertise of physicians, cell biologists, physiologists, engineers, physicists, and mathematicians, representing several institutions. Tschumperlin developed an in vitro cell culture model to mimic the conditions of the human lung when it constricts, and he detected the activation of a specific signal transduction pathway. To get a better idea of what was going on at the cell surface, Tschumperlin collaborated with groups headed by MIT biomedical engineers Peter So and Roger Kamm. The MIT scientists had unique, cutting-edge imaging tools that allowed them to reconstruct three-dimensional microscopic structures of living epithelial cells, or cells that line the airways. Another well-known MIT bioengineer, Douglas Lauffenburger, and his team worked on pinpointing the specifics of the biochemical pathway that had been detected. He developed a quantitative model to calculate the distribution of proteins among epithelial cells when the airway constricts.