listeriolysin o causes enac dysfunction in human airway epithelial cells

Clicks: 294
ID: 155074
2018
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #142 of 300 articles by views in matec web of conferences

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 300 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Pulmonary permeability edema is characterized by reduced alveolar Na+ uptake capacity and capillary barrier dysfunction and is a potentially lethal complication of listeriosis. Apical Na+ uptake is mainly mediated by the epithelial sodium channel (ENaC) and initiates alveolar liquid clearance. Here we examine how listeriolysin O (LLO), the pore-forming toxin of Listeria monocytogenes, impairs the expression and activity of ENaC. To that purpose, we studied how sub-lytic concentrations of LLO affect negative and positive regulators of ENaC expression in the H441 airway epithelial cell line. LLO reduced expression of the crucial ENaC-α subunit in H441 cells within 2 h and this was preceded by activation of PKC-α, a negative regulator of the channel’s expression. At later time points, LLO caused a significant reduction in the phosphorylation of Sgk-1 at residue T256 and of Akt-1 at residue S473, both of which are required for full activation of ENaC. The TNF-derived TIP peptide prevented LLO-mediated PKC-α activation and restored phospho-Sgk-1-T256. The TIP peptide also counteracted the observed LLO-induced decrease in amiloride-sensitive Na+ current and ENaC-α expression in H441 cells. Intratracheally instilled LLO caused profound pulmonary edema formation in mice, an effect that was prevented by the TIP peptide; thus indicating the therapeutic potential of the peptide for the treatment of pore-forming toxin-associated permeability edema.
Reference Key
yang2018toxinslisteriolysin Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Guang Yang, Helena Pillich, Richard White, Istvan Czikora, Isabelle Pochic, Qiang Yue, Martina Hudel, Boris Gorshkov, Alexander Verin, Supriya Sridhar, Carlos M. Isales, Douglas C. Eaton, Jürg Hamacher, Trinad Chakraborty, Rudolf Lucas
Are you one of these authors? Claim your profile
Journal matec web of conferences
Year 2018
DOI
10.3390/toxins10020079
URL
http://www.mdpi.com/2072-6651/10/2/79
Keywords
tnf protein kinase c-αmedicine

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.