Endotoxin upregulates expression of an antimicrobial peptide gene in mammalian airway epithelial cells

maceuticals, usually in cases of severe liver damage. The latter suggests that PIMs may be induced under certain circumstances, and we have designed these experiments to induce phagocytic pulmonary mononuclear cells in a species where they are not normally prevalent. The aims of this study were to determine whether PIMs can be induced in rats, a species normally without these cells, and whether pulmonary uptake of pathogens by such induced mononuclear cells is associated with lung injury. Rats were injected intravenously with saline solution (n=4) or 3 mg/kg Escherichia coli 0111:B4 hipopolysaccharide (LPS) (n=12). One day later, all animals were injected intravenously with a tracer particle, 5 mg/kg magnetic iron oxide (0.5 p.m diameter). One hour later, animals were humanely killed and phagocytic uptake of iron oxide in lungs, liver, and other internal organs was determined using magnetic field strength in 1 g tissue samples. A second group of saline solution control (n=6) and LPS-injected (n=6) rats was injected at 24 h with 2 x 10� colony-forming units/kg live Pseudomonas aernginosa to determine the fate of a circulating pathogenic particle. Phagocytic uptake at 1 h was determined by quantitative culture of organ samples. Lung and liver samples from each group of animals were fixed for ultrastructural study to determine the cell types responsible for iron oxide and Pseudomonas uptake. Organ distribution as the mean percent of recovered dose of iron oxide or bacteria ± SEM were: