scholarly journals MDA5 Governs the Innate Immune Response to SARS-CoV-2 in Lung Epithelial Cells

Cell Reports ◽  
2021 ◽  
Vol 34 (2) ◽  
pp. 108628 ◽  
Author(s):  
Xin Yin ◽  
Laura Riva ◽  
Yuan Pu ◽  
Laura Martin-Sancho ◽  
Jun Kanamune ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

MDA5 Governs the Innate Immune Response to SARS-CoV-2 in Lung Epithelial Cells

2020 ◽  
Author(s):  
Xin Yin ◽  
Laura Riva ◽  
Yuan Pu ◽  
Laura Martin-Sancho ◽  
Jun Kanamune ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals Interaction and Cellular Localization of the Human Host Defense Peptide LL-37 with Lung Epithelial Cells

2005 ◽  
Vol 73 (1) ◽  
pp. 583-591 ◽  
Author(s):  
Y. Elaine Lau ◽  
Annett Rozek ◽  
Monisha G. Scott ◽  
Danika L. Goosney ◽  
Donald J. Davidson ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Host Defense ◽  
Cellular Localization ◽  
Innate Immune ◽  
Lung Epithelial Cells ◽  
Perinuclear Region ◽  
Effector Cells ◽  
Host Defense Peptide

ABSTRACT LL-37 is a human cationic host defense peptide that is an essential component of innate immunity. In addition to its modest antimicrobial activity, LL-37 affects the gene expression and behavior of effector cells involved in the innate immune response, although its mode of interaction with eukaryotic cells remains unclear. The interaction of LL-37 with epithelial cells was characterized in tissue culture by using biotinylated LL-37 and confocal microscopy. It was demonstrated that LL-37 was actively taken up into A549 epithelial cells and eventually localized to the perinuclear region. Specific inhibitors were used to demonstrate that the uptake process was not mediated by actin but required elements normally involved in endocytosis and that trafficking to the perinuclear region was dependent on microtubules. By using nonlinear regression analysis, it was revealed that A549 epithelial cells have two receptors for LL-37B, with high and low affinity for LL-37, respectively. These results indicate the mode of interaction of LL-37 with epithelial cells and further our understanding of its role in modulating the innate immune response.

Innate immune response in CF airway epithelia: hyperinflammatory?

2006 ◽  
Vol 291 (2) ◽  
pp. C218-C230 ◽  
Author(s):  
Terry E. Machen
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Cellular Signaling ◽  
Basolateral Membrane ◽  
Airway Epithelial Cells ◽  
Innate Immune ◽  
Airway Epithelial ◽  
Airway Epithelia ◽  
Intracellular Ca

The lack of functional cystic fibrosis (CF) transmembrane conductance regulator (CFTR) in the apical membranes of CF airway epithelial cells abolishes cAMP-stimulated anion transport, and bacteria, eventually including Pseudomonas aeruginosa, bind to and accumulate in the mucus. Flagellin released from P. aeruginosa triggers airway epithelial Toll-like receptor 5 and subsequent NF-κB signaling and production and release of proinflammatory cytokines that recruit neutrophils to the infected region. This response has been termed hyperinflammatory because so many neutrophils accumulate; a response that damages CF lung tissue. We first review the contradictory data both for and against the idea that epithelial cells exhibit larger-than-normal proinflammatory signaling in CF compared with non-CF cells and then review proposals that might explain how reduced CFTR function could activate such proinflammatory signaling. It is concluded that apparent exaggerated innate immune response of CF airway epithelial cells may have resulted not from direct effects of CFTR on cellular signaling or inflammatory mediator production but from indirect effects resulting from the absence of CFTRs apical membrane channel function. Thus, loss of Cl−, HCO3−, and glutathione secretion may lead to reduced volume and increased acidification and oxidation of the airway surface liquid. These changes concentrate proinflammatory mediators, reduce mucociliary clearance of bacteria and subsequently activate cellular signaling. Loss of apical CFTR will also hyperpolarize basolateral membrane potentials, potentially leading to increases in cytosolic [Ca2+], intracellular Ca2+, and NF-κB signaling. This hyperinflammatory effect of CF on intracellular Ca2+and NF-κB signaling would be most prominently expressed during exposure to both P. aeruginosa and also endocrine, paracrine, or nervous agonists that activate Ca2+signaling in the airway epithelia.

An Investigation of the Innate Immune Response in Bovine Mammary Epithelial Cells Challenged by Prototheca zopfii

2016 ◽  
Vol 181 (11-12) ◽  
pp. 823-832 ◽  
Author(s):  
Zhaoju Deng ◽  
Muhammad Shahid ◽  
Limei Zhang ◽  
Jian Gao ◽  
Xiaolong Gu ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Prototheca Zopfii ◽  
Bovine Mammary Epithelial Cells
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