Effects of Lipopolysaccharide and Mannheimia haemolytica Leukotoxin on Bovine Lung Microvascular Endothelial Cells and Alveolar Epithelial Cells

摘要: Bovine respiratory disease resulting from infection with Mannheimia haemolytica commonly results in extensive vascular leakage into the alveoli. M. produces two substances, lipopolysaccharide (LPS) and leukotoxin (LKT), that are known to be important inducing some of pathological changes. In present study, we examined bovine pulmonary epithelial (BPE) cell lung microvascular endothelial monolayer permeability, as measured by trans-well electrical resistance (TEER), after incubation LPS, LKT, or LPS-activated neutrophils. Endothelial monolayers exposed LPS exhibited significant decreases TEER corresponded increased levels proinflammatory cytokines, apoptosis, morphological contrast, BPE cells production inflammatory cytokines but displayed no changes TEER, visible Both types appeared express relatively equal ligand Toll-like receptor 4. However, was decreased when were incubated Although LKT this not reduced a neutralizing antibody reversed preincubated LPS-neutralizing compound polymyxin B. Because did CD11a/CD18, infer contaminating responsible for TEER. conclusion, triggered would consistent leakage, neither nor caused similar cells, unless neutrophils also present.