Mitochondrial damage-associated molecular patterns released by abdominal trauma suppress pulmonary immune responses

Abstract

Rather than acting as a "second hit" to enhance PMN-mediated lung injury, mtDAMPs from trauma and pathogen-associated danger molecules from peritoneal infection diminish PMN accumulation in a contused lung. This may make the lung susceptible to pneumonia. This paradigm provides a novel mechanistic model of the relationship among blunt tissue trauma, systemic inflammation, and pneumonia that can be studied to improve trauma outcomes.