scholarly journals Hepoxilin A3 Facilitates Neutrophilic Breach of Lipoxygenase-Expressing Airway Epithelial Barriers

2012 ◽  
Vol 189 (10) ◽  
pp. 4960-4969 ◽  
Author(s):  
David L. Tamang ◽  
Waheed Pirzai ◽  
Gregory P. Priebe ◽  
David C. Traficante ◽  
Gerald B. Pier ◽  
...  
Keyword(s):  
Airway Epithelial ◽  
Epithelial Barriers ◽  
Hepoxilin A3

scholarly journals Staphylococcus aureus Protein A Mediates Invasion across Airway Epithelial Cells through Activation of RhoA GTPase Signaling and Proteolytic Activity

2011 ◽  
Vol 286 (41) ◽  
pp. 35891-35898 ◽  
Author(s):  
Grace Soong ◽  
Francis J. Martin ◽  
Jarin Chun ◽  
Taylor S. Cohen ◽  
Danielle S. Ahn ◽  
...  
Keyword(s):  
Egf Receptor ◽  
Protein A ◽  
Airway Epithelial Cells ◽  
Cell Junctions ◽  
Bacterial Invasion ◽  
Invasive Infection ◽  
Airway Epithelial ◽  
Calpain Activity ◽  
Epithelial Barriers

Staphyococcus aureus and especially the epidemic methicillin-resistant S. aureus strains cause severe necrotizing pneumonia. The mechanisms whereby these organisms invade across the mucosal epithelial barrier to initiate invasive infection are not well understood. Protein A (SpA), a highly conserved and abundant surface protein of S. aureus, activates TNF receptor 1 and EGF receptor (EGFR) signaling cascades that can perturb the cytoskeleton. We demonstrate that wild-type S. aureus, but not spa mutants, invade across polarized airway epithelial cell monolayers via the paracellular junctions. SpA stimulated a RhoA/ROCK/MLC cascade, resulting in the contraction of the cytoskeleton. SpA+ but not SpA− mutants stimulated activation of EGFR and along with subsequent calpain activity cleaved the membrane-spanning junctional proteins occludin and E-cadherin, facilitating staphylococcal transmigration through the cell-cell junctions. Treatment of polarized human airway epithelial monolayers with inhibitors of ROCK, EGFR, MAPKs, or calpain prevented staphylococcal penetration through the monolayers. In vivo, blocking calpain activity impeded bacterial invasion into the lung parenchyma. Thus, S. aureus exploits multiple receptors available on the airway mucosal surface to facilitate invasion across epithelial barriers.

scholarly journals The WD and linker domains of ATG16L1 required for non-canonical autophagy limit lethal respiratory infection by influenza A virus at epithelial surfaces

2020 ◽  
Author(s):  
Yingxue Wang ◽  
Weijiao Zhang ◽  
Matthew Jefferson ◽  
Parul Sharma ◽  
Ben Bone ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
High Mortality ◽  
Lung Inflammation ◽  
Influenza A ◽  
Ex Vivo ◽  
Economic Cost ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Epithelial Barriers ◽  
Innate Defence

SummaryRespiratory viruses such as influenza A virus (IAV) and SARS-CoV-2 (Covid-19) cause pandemic infections where cytokine storm syndrome, lung inflammation and pneumonia lead to high mortality. Given the high social and economic cost of these viruses, there is an urgent need for a comprehensive understanding of how the airways defend against virus infection. Viruses entering cells by endocytosis are killed when delivered to lysosomes for degradation. Lysosome delivery is facilitated by non-canonical autophagy pathways that conjugate LC3 to endo-lysosome compartments to enhance lysosome fusion. Here we use mice lacking the WD and linker domains of ATG16L1 to demonstrate that non-canonical autophagy protects mice from lethal IAV infection of the airways. Mice with systemic loss of non-canonical autophagy are exquisitely sensitive to low-pathogenicity murine-adapted IAV where extensive viral replication throughout the lungs, coupled with cytokine amplification mediated by plasmacytoid dendritic cells, leads to fulminant pneumonia, lung inflammation and high mortality. IAV infection was controlled within epithelial barriers where non-canonical autophagy slowed fusion of IAV with endosomes and reduced activation of interferon signalling. This was consistent with conditional mouse models and ex vivo analysis showing that protection against IAV infection of lung was independent of phagocytes and other leukocytes. This establishes non-canonical autophagy pathways in airway epithelial cells as a novel innate defence mechanism that can restrict IAV infection and lethal inflammation at respiratory surfaces.

New Ultrastructural Observations on Injury and Regeneration of Cilia in Mammalian Conducting Airway Epithelium

1981 ◽  
Vol 39 ◽  
pp. 624-625
Author(s):  
J.L. Carson ◽  
A.M. Collier
Keyword(s):  
Respiratory Tract ◽  
Airway Epithelium ◽  
Defense Mechanisms ◽  
Normal Growth ◽  
Fetal Lung ◽  
Secretory Cells ◽  
Airway Epithelial ◽  
Ciliated Cells ◽  
Conducting Airway ◽  
Conducting Airways

The ciliated cells lining the conducting airways of mammals are integral to the defense mechanisms of the respiratory tract, functioning in coordination with secretory cells in the removal of inhaled and cellular debris. The effects of various infectious and toxic agents on the structure and function of airway epithelial cell cilia have been studied in our laboratory, both of which have been shown to affect ciliary ultrastructure.These observations have led to questions about ciliary regeneration as well as the possible induction of ciliogenesis in response to cellular injury. Classical models of ciliogenesis in the conducting airway epithelium of the mammalian respiratory tract have been based primarily on observations of the developing fetal lung. These observations provide a plausible explanation for the embryological generation of ciliary beds lining the conducting airways but do little to account for subsequent differentiation of ciliated cells and ciliogenesis during normal growth and development.

Generation of Clara cells from murine pluripotent stem cells – a new tool to explore airway epithelial regeneration

Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
K Katsirntaki ◽  
C Mauritz ◽  
S Schmeckebier ◽  
M Sgodda ◽  
V Puppe ◽  
...  
Keyword(s):  
Stem Cells ◽  
Pluripotent Stem Cells ◽  
Airway Epithelial ◽  
Clara Cells ◽  
Epithelial Regeneration

Differentiation of human pluripotent stem cells into airway epithelial cells

Pneumologie ◽  
2015 ◽  
Vol 69 (07) ◽  
Author(s):  
S Ulrich ◽  
S Weinreich ◽  
R Haller ◽  
S Menke ◽  
R Olmer ◽  
...  
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Pluripotent Stem Cells ◽  
Airway Epithelial Cells ◽  
Human Pluripotent Stem Cells ◽  
Airway Epithelial

Priming with respiratory bacteria alters the airway epithelial response to subsequent viral infection

Pneumologie ◽  
2016 ◽  
Vol 70 (S 01) ◽  
Author(s):  
C Bellinghausen ◽  
F Gulraiz ◽  
EFM Wouters ◽  
G Rohde ◽  
FRM Stassen
Keyword(s):  
Viral Infection ◽  
Airway Epithelial

The Human Endogenous Antimicrobial Peptide Ll-37 Stimulates Airway Epithelial Repair

Pneumologie ◽  
2006 ◽  
Vol 59 (12) ◽  
Author(s):  
R Shaykhiev ◽  
C Beißwenger ◽  
K Kändler ◽  
J Senske ◽  
A Püchner ◽  
...  
Keyword(s):  
Antimicrobial Peptide ◽  
Airway Epithelial ◽  
Epithelial Repair
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