scholarly journals SARS-CoV-2 and its variants of concern infect human conjunctival epithelial cells and induce differential antiviral innate immune response

2021 ◽  
Author(s):  
Sneha Singh ◽  
Gustavo Garcia ◽  
Ruchi Shah ◽  
Andrei A. Kramerov ◽  
Robert Emery Wright ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Conjunctival Epithelial Cells

Toll-like receptor 4 initiates an innate immune response to lipopolysaccharide in human conjunctival epithelial cells

2009 ◽  
Vol 88 (1) ◽  
pp. 49-56 ◽  
Author(s):  
So-Hyang Chung ◽  
Mi-Na Kweon ◽  
Hyung Keun Lee ◽  
Seung-Il Choi ◽  
Jin-Young Yang ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Conjunctival Epithelial Cells

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

scholarly journals Innate immune response of bovine mammary epithelial cells toMycoplasma bovis

2018 ◽  
Vol 19 (1) ◽  
pp. 79 ◽  
Author(s):  
Satoshi Gondaira ◽  
Hidetoshi Higuchi ◽  
Hidetomo Iwano ◽  
Koji Nishi ◽  
Takanori Nebu ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Bovine Mammary Epithelial Cells

scholarly journals Effects of Sodium Octanoate on Innate Immune Response of Mammary Epithelial Cells duringStaphylococcus aureusInternalization

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Nayeli Alva-Murillo ◽  
Alejandra Ochoa-Zarzosa ◽  
Joel E. López-Meza
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Innate Immune Response ◽  
Mammary Epithelial Cells ◽  
Short Chain Fatty Acids ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Sodium Octanoate ◽  
Bovine Mammary Epithelial Cells

Bovine mammary epithelial cells (bMECs) are capable of initiating an innate immune response to invading bacteria. Short chain fatty acids can reduceStaphylococcus aureusinternalization into bMEC, but it has not been evaluated if octanoic acid (sodium octanoate, NaO), a medium chain fatty acid (MCFA), has similar effects. In this study we determined the effect of NaO onS. aureusinternalization into bMEC and on the modulation of innate immune elements. NaO (0.25–2 mM) did not affectS. aureusgrowth and bMEC viability, but it differentially modulated bacterial internalization into bMEC, which was induced at 0.25–0.5 mM (~60%) but inhibited at 1-2 mM (~40%). Also, bMEC showed a basal expression of all the innate immune genes evaluated, which were induced byS. aureus. NaO induced BNBD4, LAP, and BNBD10 mRNA expression, but BNBD5 and TNF-αwere inhibited. Additionally, the pretreatment of bMEC with NaO inhibited the mRNA expression induction generated by bacteria which coincides with the increase in internalization; only TAP and BNDB10 showed an increase in their expression; it coincides with the greatest effect on the reduction of bacterial internalization. In conclusion, NaO exerts a dual effect onS. aureusinternalization in bMEC and modulates elements of innate immune response.

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