The loss of the inflammatory protein TREM-1 increased inflammation in the lungs of mice infected with pneumonia, making them more likely to die from lung infection, according to research in the Journal of Clinical Investigation.
Neutrophils, which play an essential role in the innate immune response to lung infection, “have an armamentarium of pattern recognition molecules and antimicrobial agents that identify and eliminate pathogens,” according to researchers.
Researcher demonstrated that when an infection is present, triggering receptor expressed on myeloid cells 1 (TREM-1) plays an important role in transepithelial migration of neutrophils into the airspace. Investigators developed a TREM-1/3–deficient mouse model of pneumonia and found that absence of TREM-1/3 markedly increased mortality following exposure to Pseudomonas aeruginosa. The deficiency also increased local and systemic cytokine production.
“TREM-1/3–deficient neutrophils demonstrated intact bacterial killing, phagocytosis, and chemotaxis; however, histologic examination of TREM-1/3–deficient lungs revealed decreased neutrophil infiltration of the airways,” the authors wrote. “TREM-1/3–deficient neutrophils effectively migrated across primary endothelial cell monolayers but failed to migrate across primary airway epithelia grown at the air-liquid interface.”
According to researchers, the results “define a new function for TREM-1 in neutrophil migration across airway epithelial cells and suggest that it amplifies inflammation through targeted neutrophil migration into the lung.”
