Anti-Inflammatory Peptide Protects Against Acute Respiratory Distress Syndrome

These animals were then treated either with a placebo or with delta-PKC TAT inhibitory peptide. This peptide inhibits the activity of the enzyme delta-protein kinase C (delta-PKC). Delta-PCK regulates proinflammatory signaling in neutrophils and endothelial and epithelial cells, cells that can contribute to lung tissue damage associated with inflammation.

Results published in the January 2011 issue of the Journal of Leukocyte Biology revealed that the 2CLP procedure induced delta-PKC phosphorylation in the lung within 24 hours. However, treatment with delta-PKC TAT inhibitory peptide significantly decreased pulmonary delta-PKC phosphorylation, indicating effective inhibition of delta-PKC activation. At the cellular level administration of delta-PKC TAT peptide significantly reduced inflammatory cell infiltration, disruption of lung architecture, and pulmonary edema associated with 2CLP.

"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 first author Dr. Laurie E. Kilpatrick, associate professor of physiology at Temple University. "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."

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