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| | | ![]() Key Peptide Responsible In Cystic Fibrosis-Associated Lung Infection PLYMOUTH MEETING, Pa., Feb. 21, 1997 -- Researchers report critical evidence that inactivation of a natural antibiotic peptide is responsible for life-threatening lung infections in cystic fibrosis patients. In a paper published today in the journal Cell, scientists at Magainin Pharmaceuticals Inc. (Nasdaq: MAGN), along with collaborators at the University of Pennsylvania report this important finding regarding the role of a key peptide, human beta-defensin-1 (HBD-1), in mediating the onset of lung infection in cystic fibrosis patients. This finding further supports the concept of developing a therapeutic to replace HBD-1 for the treatment and prevention of lung infection. Early studies that aided in the discovery of HBD-1 were supported by the Cystic Fibrosis Foundation. The reason for cystic fibrosis patients' high susceptibility to serious infection, resulting in lung destruction, has always been unclear. In today's publication, scientists collaborating at Magainin and Penn have now shown that, in healthy subjects, HBD-1 acts as a natural antibiotic, protecting the lung from infection. In cystic fibrosis, however, an increase in the amount of salt present on the surface of the lung bronchial tubes, inactivates this natural defense system. As reported by Goldman et. al., [Cell 88:1-20 (1997)], inactivation of HBD-1 was recreated in a bronchial xenograft model and shown to promote the lung infections typical of cystic fibrosis.
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