Effects of Lipopolysaccharide andMannheimia haemolyticaLeukotoxin on Bovine Lung Microvascular Endothelial Cells and Alveolar Epithelial Cells
- 1 February 2008
- journal article
- Published by American Society for Microbiology in Clinical and Vaccine Immunology
- Vol. 15 (2), 338-347
- https://doi.org/10.1128/cvi.00344-07
Abstract
Bovine respiratory disease resulting from infection with Mannheimia haemolytica commonly results in extensive vascular leakage into the alveoli. M. haemolytica produces two substances, lipopolysaccharide (LPS) and leukotoxin (LKT), that are known to be important in inducing some of the pathological changes. In the present study, we examined bovine pulmonary epithelial (BPE) cell and bovine lung microvascular endothelial cell monolayer permeability, as measured by trans-well endothelial and epithelial cell electrical resistance (TEER), after incubation with LPS, LKT, or LPS-activated neutrophils. Endothelial cell monolayers exposed to LPS exhibited significant decreases in TEER that corresponded with increased levels of proinflammatory cytokines, apoptosis, and morphological changes. In contrast, BPE cells exposed to LPS increased the levels of production of inflammatory cytokines but displayed no changes in TEER, apoptosis, or visible morphological changes. Both cell types appeared to express relatively equal levels of the LPS ligand Toll-like receptor 4. However, TEER in BPE cell monolayers was decreased when the cells were incubated with LPS-activated neutrophils. Although the incubation of BPE cells with LKT decreased TEER, this was not reduced by the incubation of LKT with a neutralizing antibody and was reversed when LKT was preincubated with the LPS-neutralizing compound polymyxin B. Because BPE cells did not express the LKT receptor CD11a/CD18, we infer that contaminating LPS was responsible for the decreased TEER. In conclusion, LPS triggered changes in endothelial cells that would be consistent with vascular leakage, but neither LPS nor LKT caused similar changes in epithelial cells, unless neutrophils were also present.Keywords
This publication has 51 references indexed in Scilit:
- Up-regulation interleukin-6 and interleukin-8 by activated protein C in lipopolysaccharide-treated human umbilical vein endothelial cellsJournal of Zhejiang University-SCIENCE B, 2006
- NF-κB regulation of endothelial cell function during LPS-induced toxemia and cancerJCI Insight, 2006
- Lipopolysaccharide-stimulated responses in rat aortic endothelial cells by a systems biology approachProteomics, 2006
- Lipopolysaccharide-induced decreased protein S expression in liver cells is mediated by MEK/ERK signaling and NFκB activation: involvement of membrane-bound CD14 and toll-like receptor-4Journal of Thrombosis and Haemostasis, 2006
- Modulation of endothelial monolayer permeability induced by plasma obtained from lipopolysaccharide-stimulated whole bloodClinical and Experimental Immunology, 2006
- Mannheimia haemolytica Leukotoxin Induces Apoptosis of Bovine Lymphoblastoid Cells (BL-3) via a Caspase-9-Dependent Mitochondrial PathwayInfection and Immunity, 2005
- Nitrite enhances neutrophil-induced DNA strand breakage in pulmonary epithelial cells by inhibition of myeloperoxidaseCarcinogenesis: Integrative Cancer Research, 2005
- Endotoxin responsiveness of human airway epithelia is limited by low expression of MD-2American Journal of Physiology-Lung Cellular and Molecular Physiology, 2004
- TIRAP mediates endotoxin-induced NF-κB activation and apoptosis in endothelial cellsBiochemical and Biophysical Research Communications, 2002
- EXOGENOUS CATALASE MAY POTENTIATE OXIDANT-MEDIATED LUNG INJURY IN THE FEMALE SPRAGUE-DAWLEY RATJournal of Toxicology and Environmental Health, 1996