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Archive - Mar 31, 2013

New Finding Could Aid Treatment of Pneumonia and Other Inflammatory Diseases

Scientists at the University of Pittsburgh (Pitt) School of Medicine and Veterans Affairs Pittsburgh Health System have discovered a new biological pathway of innate immunity that ramps up inflammation and then identified agents that can block the pathway, leading to increased survival and improved lung function in animal models of pneumonia. They reported their findings online on March 31, 2013 in Nature Immunology. Pneumonia and other infections sometimes provoke an inflammatory response from the body that is more detrimental than the disease-causing bacteria, said senior author Rama Mallampalli, M.D, professor and vice chair for research, Department of Medicine, and director of the Acute Lung Injury Center of Excellence at Pitt. "In our ongoing studies of pneumonia, we found infecting bacteria activate a previously unknown protein called Fbxo3 to form a complex that degrades another protein called Fbxl2, which is needed to suppress the inflammatory response," said Dr. Mallampalli, who is also chief of the pulmonary division of the VA Pittsburgh Healthcare System. "The result is an exaggerated inflammatory response that can lead to further damage of the lung tissue, multi-organ failure, and shock." The research team, led by Bill B. Chen, Ph.D., associate professor, Division of Pulmonary, Allergy, and Critical Care Medicine, conducted experiments in which mice that lacked the ability to make Fbxo3 were infected with a strain of Pseudomonas bacteria, and found that the mice had better lung mechanics and longer survival times than mice that still made the protein. Research team members Bryan J.

New Clues to Development of ALS (Lou Gehrig’s Disease)

Johns Hopkins scientists and colleagues say they have evidence from animal studies that a type of central nervous system cell other than motor neurons plays a fundamental role in the development of amyotrophic lateral sclerosis (ALS), a fatal degenerative disease. The discovery holds promise, they say, for identifying new targets for interrupting the disease's progress. In a study described online on March 31, 2013 in Nature Neuroscience, the researchers found that, in mice bred with a gene mutation that causes human ALS, dramatic changes occurred in oligodendrocytes — cells that create insulation for the nerves of the central nervous system — long before the first physical symptoms of the disease appeared. Oligodendrocytes located near motor neurons — cells that govern movement — died off at very high rates, and new ones regenerated in their place were inferior and unhealthy. The researchers also found, to their surprise, that suppressing an ALS-causing gene in oligodendrocytes of mice bred with the disease — while still allowing the gene to remain in the motor neurons — profoundly delayed the onset of ALS. It also prolonged survival of these mice by more than three months, a long time in the life span of a mouse. These observations suggest that oligodendrocytes play a very significant role in the early stage of the disease. "The abnormalities in oligodendrocytes appear to be having a negative impact on the survival of motor neurons," says Dwight E. Bergles, Ph.D., a co-author of the article and a professor of neuroscience at the Johns Hopkins University School of Medicine.