Faculty Publications

Effect Of TRIF On Permeability And Apoptosis In Bovine Microvascular Endothelial Cells Exposed To Lipopolysaccharide

Document Type

Article

Keywords

Bovine, Lipopolysaccharide, Microvascular endothelial cells, MyD88, Toll-like receptor 4, TRIF

Journal/Book/Conference Title

Veterinary Journal

Volume

198

Issue

2

First Page

419

Last Page

423

Abstract

Bovine respiratory disease complex (BRDC) can be caused by several Gram negative bacteria. Lung endothelial cells may be damaged by the release of lipopolysaccharide (LPS) from these organisms. Toll-like receptor (TLR-4) signaling pathways include the myeloid differentiation primary response gene 88 (MyD88) and the Toll/interleukin (IL)-1 receptor (TIR) domain-containing adapter-inducing interferon-β (TRIF) pathways. The aim of this study was to determine which of these pathways is responsible for permeability changes, apoptosis and cytokine production in bovine lung microvascular cells exposed to LPS. Bovine lung endothelial cells were treated with a peptide to inhibit MyD88 signaling or small interfering RNA (siRNA) to inhibit TRIF signaling. Effects were measured using trans-well endothelial electrical resistance to determine cell monolayer permeability, annexin staining to estimate apoptosis and real-time PCR to measure levels of expression of IL-1β and tumor necrosis factor (TNF)-α mRNA. Inhibition of TRIF signaling reduced permeability changes and apoptosis in endothelial cells exposed to LPS. In contrast, MyD88 inhibition reduced expression of IL-1β and TNF-α mRNA in LPS treated cells, but had no effect on permeability. It was concluded that TRIF signaling in LPS-stimulated lung endothelial cells results in permeability changes and apoptosis. © 2013 Elsevier Ltd.

Department

Department of Biology

Original Publication Date

11-1-2013

DOI of published version

10.1016/j.tvjl.2013.08.025

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