Intratracheal instillation of lipopolysaccharide in mice induces apoptosis in bronchial epithelial cells: no role for tumor necrosis factor-alpha and infiltrating neutrophils.

摘要: This study investigated apoptosis in lungs after local exposure to lipopolysaccharide (LPS). Mice were instilled intratracheally with 5 microg LPS, which corresponds the amount acquired by smoking approximately 25 cigarettes, and killed at different time points exposure. Our data demonstrate that LPS resulted from 2 h peaked 24 h, as detected ligation-mediated polymerase chain reaction. Morphologic examination terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end label staining demonstrated bronchial epithelial cells early intratracheal (IT) challenge, whereas infiltrating neutrophils displayed positive 72 Apoptosis clearly preceded pulmonary neutrophil infiltration, confirming did not contribute points. Further, using three experimental approaches--namely, anti-tumor necrosis factor (TNF)-alpha treatment, IT TNF-alpha instillation, TNF/lymphotoxin-alpha knockout mice--we TNF-alpha, was elevated both messenger RNA protein levels no primary mediator LPS-induced Thus, mice of independent suggests epithelium may be involved airway injury during LPS.