From these findings, they reasoned that oxygen therapy given to patients with acute lung inflammation might "short-circuit" this protective pathway by preventing oxygen levels from dropping enough to trigger the inflammation stop signal.
To explore this possibility in an animal model, Dr. Sitkovsky and his colleagues induced lung inflammation in three groups of mice. The first group of 15 mice did not receive any supplemental oxygen. While they sustained moderate lung damage, only two died. Another group of 15 mice with acute lung inflammation were treated with either 100 percent or 60 percent oxygen for 48 hours. These mice suffered very extensive lung damage, and 11 of 15 died. Finally, the scientists treated another 15 mice with acute lung inflammation with a combination of 100 percent oxygen and an adenosine-like drug to compensate for the oxygen-induced loss of natural adenosine. Only two mice in this group died, and exacerbation of lung inflammation by oxygen was prevented.
The investigators conclude that in this small animal model highly pure oxygen therapy without the addition of an adenosine substitute worsens pre-existing lung inflammation. "We suggest that these adenosine substitutes be evaluated for their possible usefulness in settings of acute lung inflammation due to infection or other causes, such as asthma or surgical trauma," says Dr. Sitkovsky.
Dr. Sitkovsky is now continuing his research at the newly established New England Inflammation and Tissue Protection Institute, a consortium at Northeastern University in Boston.
NIAID is a component of the National Institutes of Health, an agency of the U.S. Department of Health and Human Services. NIAID supports basic and applied research to prevent, diagnose and treat infectious diseases such as HIV/AIDS and other sexually transmitted infections, influenza, tuberculosis, malaria and illness from potential agents of bi
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Contact: Anne A. Oplinger
aoplinger@niaid.nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
2-May-2005