MCPIP1 attenuates the innate immune response to influenza A virus by suppressing RIG-I expression in lung epithelial cells

2017 ◽  
Vol 90 (2) ◽  
pp. 204-211 ◽  
Author(s):  
Xiaoning Sun ◽  
Wenjing Feng ◽  
Yidi Guo ◽  
Qi Wang ◽  
Chunyan Dong ◽  
...  
Cell Reports ◽  
2021 ◽  
Vol 34 (2) ◽  
pp. 108628 ◽  
Author(s):  
Xin Yin ◽  
Laura Riva ◽  
Yuan Pu ◽  
Laura Martin-Sancho ◽  
Jun Kanamune ◽  
...  

2020 ◽  
Author(s):  
Xin Yin ◽  
Laura Riva ◽  
Yuan Pu ◽  
Laura Martin-Sancho ◽  
Jun Kanamune ◽  
...  

2004 ◽  
Vol 280 (7) ◽  
pp. 5571-5580 ◽  
Author(s):  
Loïc Guillot ◽  
Ronan Le Goffic ◽  
Sarah Bloch ◽  
Nicolas Escriou ◽  
Shizuo Akira ◽  
...  

2002 ◽  
Vol 76 (18) ◽  
pp. 9298-9306 ◽  
Author(s):  
Ute Arndt ◽  
Gunther Wennemuth ◽  
Peter Barth ◽  
Marianne Nain ◽  
Yousef Al-Abed ◽  
...  

ABSTRACT Bronchiolar epithelial cells are the prime targets for influenza A virus infection. It still remains to be clarified which signals are generated from these cells to initiate an immune response. Among chemokines, viral infection of primary lung epithelial cells triggered exclusively the release of CXCL8/interleukin-8 (IL-8), which contrasts with our previous observation that influenza A virus induced in monocytes the expression of mononuclear-leukocyte-attracting chemokines and even suppressed the production of neutrophil-attracting chemokines. Therefore, we speculated that it may be advantageous for respiratory epithelial cells to release primarily neutrophil-attracting CXCL8/IL-8 since neutrophils rapidly remove necrotic debris and are the first line of defense against bacterial superinfections. This concept has also been supported by our finding that influenza A virus infection led to necrosis of lung epithelial cells. This is in striking contrast to previous studies where influenza A virus infection induced apoptosis in monocytes and epithelial cells from origins other than the lung. Thus, the cell type instead of the virus determines which death pathway will be followed. In addition to the release of CXCL8/IL-8, we obtained a massive release of macrophage migration inhibitory factor (MIF) from virus-infected lung cells. However, whereas the CXCL8/IL-8 secretion was accompanied by induced gene activation, the transcription rate of MIF remained unchanged during the infection course and the virus-induced MIF release was predominantly a discharge from intracellular stores, suggesting that MIF is passively released upon cell death. Despite virus induced necrosis, the passively liberated MIF remained bioactive. Considering the well-established immunostimulatory effects of MIF on different leukocyte subsets, is its very likely that enhanced levels of MIF may contribute to the host immune response during the acute phase of influenza A virus infection in humans.


2016 ◽  
Vol 8 (17) ◽  
pp. 2017-2031 ◽  
Author(s):  
Simona Panella ◽  
Maria Elena Marcocci ◽  
Ignacio Celestino ◽  
Sergio Valente ◽  
Clemens Zwergel ◽  
...  

2012 ◽  
Vol 86 (18) ◽  
pp. 10211-10217 ◽  
Author(s):  
Andrea Rückle ◽  
Emanuel Haasbach ◽  
Ilkka Julkunen ◽  
Oliver Planz ◽  
Christina Ehrhardt ◽  
...  

Influenza A virus (IAV) infection of epithelial cells activates NF-κB transcription factors via the canonical NF-κB signaling pathway, which modulates both the antiviral immune response and viral replication. Since almost nothing is known so far about a function of noncanonical NF-κB signaling after IAV infection, we tested infected cells for activation of p52 and RelB. We show that the viral NS1 protein strongly inhibits RIG-I-mediated noncanonical NF-κB activation and expression of the noncanonical target gene CCL19.


2019 ◽  
Vol 61 (3) ◽  
pp. 395-398
Author(s):  
Christin Peteranderl ◽  
Irina Kuznetsova ◽  
Jessica Schulze ◽  
Martin Hardt ◽  
Emilia Lecuona ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document