Mechanisms of Hypoxemia in Acute Lung Injury
The Jones Laboratory is interested in understanding the role of IL-1b as an independent determinant of low oxygen levels during acute lung injury. In our mouse model, we generate lung injury using a combination of a bacterial toxin called LPS and mechanical ventilation. The Jones Lab has found that mice that do not make IL-1b have the same amount of inflammatory lung injury, but do not develop low oxygen levels typically found in this model.
Blood flow in the lungs of mouse models treated with the bacterial toxin LPS to induce acute lung injury (right) is significantly reduced compared with untreated mice, as shown in SPECT images.
The Jones Lab hypothesizes that abnormal blood flow in the lungs may be a part of this phenomenon. Therefore, the Jones Lab is using a mouse that has green fluorescent protein only in the cells that regulate pulmonary blood flow (vascular smooth muscle cells) to understand how IL-1b may be playing a role in this disease. The Jones Laboratory is also using novel in vivo imaging techniques to try to determine the functional changes that occur during the development of acute lung injury.
Lung section of a genetically engineered mouse that expresses green fluorescent protein in vascular smooth muscle cells only. All other cells express red fluorescent protein.