Control of the Pneumocystis life cycle
Our laboratory has been engaged in better understanding the mechanism by which Pneumocystis organisms proliferate in the lungs. We have cloned and characterized important cell cycle regulatory proteins, including CDC2 and CDC25. In addition, we are currently engaged in understanding signaling mechanisms, which are activated when Pneumocystis interacts with lung epithelium. The binding of Pneumocystis to lung epithelium appears to be a cognate portion of the organisms’ life cycle promoting organism mating and proliferation.
Mechanisms of lung inflammation in Pneumocystis pneumonia
Our laboratory has also focused on mechanisms by which lung inflammation is elicited during Pneumocystis infection. Exuberant inflammation is actually more damaging to lung function than toxic effects of the organisms themselves. We have focused upon interactions of cell surface beta glucans with alveolar macrophages in epithelial cells through a variety of innate immune receptors. These studies target new mechanisms to control lung inflammation during Pneumocystis pneumonia.
Mechanisms of lung fibrosis in idiopathic pulmonary fibrosis
Our laboratory is currently engaged in collecting human tissues of patients with usual interstitial pneumonia and nonspecific interstitial pneumonia, the two most important variants of idiopathic pulmonary fibrosis. We are studying cell signaling mechanisms that mediate fibrosis both through tumor necrosis factor alpha activation as well as through transforming growth factor beta. Through a combination of studies on human tissues, cell culture, and animal modeling (including bleomycin fibrosis models) we aim to develop new agents to treat this important cause of lung damage.
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