INTERLEUKIN 13

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Severe asthma makes up a small, but expensive and difficult to treat portion of the asthma population. Little is known about its pathogenesis. Some evidence suggests that severe asthmatics may have lost some of the elastic properties of their lungs, predisposing the airways to collapse. This is similar to what occurs in people with emphysema, yet the inflammatory processes that drive the two diseases appear to be quite different. Preliminary data from our laboratory suggest that the lungs from patients with severe asthma have evidence for changes in elastin, a protein that contributes to elastic properties of the lungs, that are similar to those seen in emphysema. These changes appear to be most prominent in the small airways and alveolar (air sac) attachments. Additionally, myofibroblasts, cells that are prominent in healing wounds, also appear to be increased in severe asthma, but again, primarily in the distal portion of the lung. The cytokine, interleukin 13 may play a role in modulating some of these changes by up-regulating a protein, matrix metalloproteinase 12, which has been found in association with models of emphysema. We propose to study the distal portion of the lungs through transbronchial biopsies and bronchoalveolar lavage, in patients with a wide range of asthma severity, to evaluate the differences in IL-13, myofibroblasts, elastin and the loss of elasticity of the lungs.