Every year, more than 200, 000 Americans die from sepsis, a severe illness caused by bacterial infection of the bloodstream. A study by Vikas Sukhatme and colleagues (Beth Israel Deaconess Medical Center and Harvard Medical School) now reveals that a protein called angiopoietin-2 may play a pivotal role in acute respiratory distress syndrome (ARDS), a condition that affects about 40% of patients with sepsis and worsens their prognosis.

In ARDS, small blood vessels in the lungs become leaky and release fluid. This impairs lung function, and patients experience trouble breathing and need to be put on respirators. If the condition lasts too long, the lung tissue gets damaged irreversibly. But what causes the leakage of fluid out of the blood vessels?

Blood vessels are normally lined with tightly linked cells, called endothelial cells, that form an impermeable barrier. Animal experiments had suggested that the development of this barrier is controlled by two small proteins called angiopoietin-1 (Ang-1) and angoipoietin-2 (Ang-2) together with these proteins' receptor, called Tie 2. These experiments also suggested that Ang-2 might disrupt the barrier lining the blood vessel wall. These and other observations prompted Sukhatme's team to ask whether the Tie-2 signaling pathway is affected in sepsis and, specifically, whether excess Ang-2 levels might promote the leakage of fluid from the blood vessels that underlies ARDS.

They tested whether excess levels of Ang-2 occur in sepsis and could cause leakiness of lung blood vessels in three different ways: First, they measured the level of Ang-2 in the blood of patients with sepsis. Second, they tested whether blood from patients with sepsis could cause leakiness in blood vessels grown in the laboratory. Finally, they tested whether elevated levels of Ang-2 affect the permeability of lung blood vessels in mice. They found that Ang-2 levels are elevated in patients with sepsis, especially in those w
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Contact: Paul Ocampo
press@plos.org
415-624-1224
Public Library of Science
23-Jan-2006

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