Inhibition of anti-viral responses in intestinal epithelial cells by epigenetic modifying drugs is mediated by a reduction in viral pattern recognition receptor expression and activity

2019 ◽  
Vol 41 (5) ◽  
pp. 527-537
Author(s):  
Conor Hennessy ◽  
Sarah O’Connell ◽  
Laurence J. Egan ◽  
Declan P. McKernan
2006 ◽  
Vol 177 (2) ◽  
pp. 1007-1016 ◽  
Author(s):  
François-Xavier Hubert ◽  
Cécile Voisine ◽  
Cédric Louvet ◽  
Jean-Marie Heslan ◽  
Asmahan Ouabed ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mandy Menzel ◽  
Joakim Kosinski ◽  
Lena Uller ◽  
Hamid Akbarshahi

Abstract Macrophages play an important role in asthma pathogenesis both in the inflammatory and resolution phase of the disease. Macrophages can acquire different polarisation states dependent on their microenvironment. It is yet unclear through which mechanism the microenvironment affects the anti-viral response in macrophages. We hypothesized that the macrophage microenvironment regulates rhinovirus-induced IFNβ expression. Murine bone marrow-derived monocytes and human differentiated THP-1 cells were stimulated with M-CSF or GM-CSF and IFNγ or IL-4/IL-13, respectively, to mimic a Th1 or Th2 environment. Macrophages were infected with rhinovirus and gene and protein levels of IFNβ and pattern recognition receptor expression were measured. In subsequent experiments an IκB kinase inhibitor was used to study the involvement of NFκB. Both murine and human M1-like macrophages exhibited higher levels of IFNβ and pattern recognition receptors after rhinovirus infection than M2-like macrophages. Blockage of NFκB resulted in a lower expression of rhinovirus-induced IFNβ in human M1-like macrophages while inducing a higher expression in M2-like macrophages, suggesting that the interferon response towards viral infection was mediated by NFκB. These findings could contribute to a better understanding of mechanisms causing reduced anti-viral responses at viral-induced exacerbations in asthma.


2001 ◽  
Vol 269 (1) ◽  
pp. 109-116 ◽  
Author(s):  
Christopher C.M. Waterhouse ◽  
Robbie R. Joseph ◽  
Andrew W. Stadnyk

2019 ◽  
Vol 101 (4) ◽  
pp. 733-747 ◽  
Author(s):  
Maolei Gong ◽  
Fei Wang ◽  
Weihua Liu ◽  
Ran Chen ◽  
Han Wu ◽  
...  

Abstract The seminal vesicles can be infected by microorganisms, thereby resulting in vesiculitis and impairment in male fertility. Innate immune responses in seminal vesicles cells to microbial infections, which facilitate vesiculitis, have yet to be investigated. The present study aims to elucidate pattern recognition receptor–mediated innate immune responses in seminal vesicles epithelial cells. Various pattern recognition receptors, including Toll-like receptor 3, Toll-like receptor 4, cytosolic ribonucleic acid, and deoxyribonucleic acid sensors, are abundantly expressed in seminal vesicles epithelial cells. These pattern recognition receptors can recognize their respective ligands, thus activating nuclear factor kappa B and interferon regulatory factor 3. The pattern recognition receptor signaling induces expression of pro-inflammatory cytokines, such as tumor necrosis factor alpha (Tnfa) and interleukin 6 (Il6), chemokines monocyte chemoattractant protein-1 (Mcp1) and C–X–C motif chemokine 10 (Cxcl10), and type 1 interferons Ifna and Ifnb. Moreover, pattern recognition receptor-mediated innate immune responses up-regulated the expression of microsomal prostaglandin E synthase and cyclooxygenase 2, but they down-regulated semenogelin-1 expression. These results provide novel insights into the mechanism underlying vesiculitis and its impact on the functions of the seminal vesicles.


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