Moraxella catarrhalis decreases antiviral innate immune responses by down‐regulation of TLR3 via inhibition of p53 in human bronchial epithelial cells

2016 ◽  
Vol 30 (6) ◽  
pp. 2426-2434 ◽  
Author(s):  
Annina Heinrich ◽  
Helge Haarmann ◽  
Sabrina Zahradnik ◽  
Katrin Frenzel ◽  
Frauke Schreiber ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Moraxella Catarrhalis ◽  
Bronchial Epithelial Cells ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Human Bronchial Epithelial Cells ◽  
Down Regulation ◽  
Bronchial Epithelial

Comparison of innate immune responses towards rhinovirus infection of primary nasal and bronchial epithelial cells

Respirology ◽  
2015 ◽  
Vol 21 (2) ◽  
pp. 304-312 ◽  
Author(s):  
Marco P. Alves ◽  
Aline Schögler ◽  
Simone Ebener ◽  
Nathalie J. Vielle ◽  
Carmen Casaulta ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Bronchial Epithelial Cells ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Bronchial Epithelial ◽  
Rhinovirus Infection

Carbocysteine regulates innate immune responses and senescence processes in cigarette smoke stimulated bronchial epithelial cells

2013 ◽  
Vol 223 (2) ◽  
pp. 198-204 ◽  
Author(s):  
Elisabetta Pace ◽  
Maria Ferraro ◽  
Liboria Siena ◽  
Valeria Scafidi ◽  
Stefania Gerbino ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Cigarette Smoke ◽  
Bronchial Epithelial Cells ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Bronchial Epithelial

scholarly journals Pseudomonas aeruginosa Suppresses Interferon Response to Rhinovirus Infection in Cystic Fibrosis but Not in Normal Bronchial Epithelial Cells

2011 ◽  
Vol 79 (10) ◽  
pp. 4131-4145 ◽  
Author(s):  
Sangbrita S. Chattoraj ◽  
Shyamala Ganesan ◽  
Andrea Faris ◽  
Adam Comstock ◽  
Wai-Ming Lee ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Bronchial Epithelial Cells ◽  
Innate Immune ◽  
Interferon Response ◽  
Innate Immune Responses ◽  
Normal Cells ◽  
Bronchial Epithelial ◽  
Content Type ◽  
Infected Cells

ABSTRACTDespite increased morbidity associated with secondary respiratory viral infections in cystic fibrosis (CF) patients with chronicPseudomonas aeruginosainfection, the underlying mechanisms are not well understood. Here, we investigated the effect ofP. aeruginosainfection on the innate immune responses of bronchial epithelial cells to rhinovirus (RV) infection. CF cells sequentially infected with mucoidP. aeruginosa(MPA) and RV showed lower levels of interferons (IFNs) and higher viral loads than those of RV-infected cells. Unlike results for CF cells, normal bronchial epithelial cells coinfected with MPA/RV showed higher IFN expression than RV-infected cells. In both CF and normal cells, the RV-stimulated IFN response requires phosphorylation of Akt and interferon response factor 3 (IRF3). Preinfection with MPA inhibited RV-stimulated Akt phosphorylation and decreased IRF3 phosphorylation in CF cells but not in normal cells. Compared to normal, unstimulated CF cells or normal cells treated with CFTR inhibitor showed increased reactive oxygen species (ROS) production. Treatment of CF cells with antioxidants prior to MPA infection partially reversed the suppressive effect of MPA on the RV-stimulated IFN response. Together, these results suggest that MPA preinfection inhibits viral clearance by suppressing the antiviral response particularly in CF cells but not in normal cells. Further, increased oxidative stress in CF cells appears to modulate the innate immune responses to coinfection.

scholarly journals Human coronaviruses 229E and OC43 replicate and induce distinct antiviral responses in differentiated primary human bronchial epithelial cells

2020 ◽  
Vol 319 (6) ◽  
pp. L926-L931
Author(s):  
Su-Ling Loo ◽  
Peter A. B. Wark ◽  
Camille Esneau ◽  
Kristy S. Nichol ◽  
Alan C-Y. Hsu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Time Course ◽  
Bronchial Epithelial Cells ◽  
Innate Immune ◽  
Infection Model ◽  
Type I ◽  
Human Bronchial Epithelial Cells ◽  
Cell Infection ◽  
Bronchial Epithelial ◽  
Human Coronaviruses

The recurrent emergence of novel, pathogenic coronaviruses (CoVs) severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1; 2002), Middle East respiratory syndrome (MERS)-CoV (2012), and most recently SARS-CoV-2 (2019) has highlighted the need for physiologically informative airway epithelial cell infection models for studying immunity to CoVs and development of antiviral therapies. To address this, we developed an in vitro infection model for two human coronaviruses; alphacoronavirus 229E-CoV (229E) and betacoronavirus OC43-CoV (OC43) in differentiated primary human bronchial epithelial cells (pBECs). Primary BECs from healthy subjects were grown at air-liquid interface (ALI) and infected with 229E or OC43, and replication kinetics and time-course expression of innate immune mediators were assessed. OC43 and 229E-CoVs replicated in differentiated pBECs but displayed distinct replication kinetics: 229E replicated rapidly with viral load peaking at 24 h postinfection, while OC43 replication was slower peaking at 96 h after infection. This was associated with diverse antiviral response profiles defined by increased expression of type I/III interferons and interferon-stimulated genes (ISGs) by 229E compared with no innate immune activation with OC43 infection. Understanding the host-virus interaction for previously established coronaviruses will give insight into pathogenic mechanisms underpinning SARS-CoV-2-induced respiratory disease and other future coronaviruses that may arise from zoonotic sources.

Sign in / Sign up

Export Citation Format

Share Document