All of us may be able to breathe a little easier now that scientists from Pennsylvania have found a new therapeutic target for controlling dangerous inflammation in the lungs. A new research report in the January 2011 issue of the Journal of Leukocyte Biology (http://www.jleukbio.org) suggests that blocking the activation of an enzyme called delta-protein kinase C (delta-PKC) could protect the lungs from neutrophil-mediated damage, which can result in out of control inflammation. In an animal model of acute respiratory distress syndrome (ARDS), inhibiting delta-PKC in the lungs showed dramatically reduced inflammation, thereby protecting the lungs from further damage.
"ARDS is a major public health problem and one of the leading causes of death in intensive care units. It is characterized by excessive pulmonary inflammation and neutrophil infiltrations of the lung," said Laurie E. Kilpatrick, Ph.D., co author of the study from the Center for Inflammation, Translational and Clinical Lung Research and Department of Physiology at Temple University School of Medicine in Philadelphia. "While no specific pharmacologic therapeutics are available to treat this disease, control of delta-PKC activity may offer a unique therapeutic target for the treatment of ARDS and prevent the significant morbidity and mortality associated with sepsis and trauma."
To make this discovery, Kilpatrick and colleagues used a rat model of severe inflammation or sepsis that produces lung injury. The animals were divided into two groups; one group received the inhibitor directly into the lungs and the other group received a placebo. After 24 hours, the placebo group showed signs of lung injury and illness, lung tissue damage and breathing problems. In contrast, the group that received the delta-PKC inhibitor had markedly reduced evidence of lung injury and distress. These results suggest that delta-PKC is an important regulator
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