scholarly journals Innate antiviral cytokine response to swine influenza virus by swine respiratory epithelial cells

2021 ◽  
Author(s):  
Abhijeet Bakre ◽  
Les Jones ◽  
Jackelyn Murray ◽  
Z. Beau Reneer ◽  
Victoria Meliopoulos ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Epithelial Cells ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Cytokine Response ◽  
Cell Type ◽  
Respiratory Epithelial Cells ◽  
Interferon Stimulated Genes ◽  
Virus Reassortment ◽  
Respiratory Epithelial

Swine influenza virus (SIV) can cause respiratory illness in swine. Swine contribute to influenza virus reassortment as avian, human, and/or SIV viruses can infect swine, reassort, and new viruses can emerge. Thus, it is important to determine the host antiviral responses that affect SIV replication. In this study, we examined the innate antiviral cytokine response to SIV by swine respiratory epithelial cells focusing on the expression of interferon (IFN) and interferon-stimulated genes (ISGs). Both primary and transformed swine nasal and tracheal respiratory epithelial cells were examined following infection with field isolates. The results show IFN and ISG expression is maximal at 12-hour post-infection (hpi) and is cell-type and virus genotype-dependent. Importance Swine are considered intermediate hosts that have facilitated influenza virus reassortment events that have given rise pandemics or genetically related viruses have become established in swine. In this study, we examine the innate antiviral response to swine influenza virus in primary and immortalized swine nasal and tracheal epithelial cells, and show virus strain and host cell-type dependent differential expression of key interferons and interferon-stimulated genes.

scholarly journals Primary Swine Respiratory Epithelial Cell Lines for the Efficient Isolation and Propagation of Influenza A Viruses

2020 ◽  
Vol 94 (24) ◽  
Author(s):  
Victoria Meliopoulos ◽  
Sean Cherry ◽  
Nicholas Wohlgemuth ◽  
Rebekah Honce ◽  
Karen Barnard ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Epithelial Cells ◽  
Cell Lines ◽  
Influenza A ◽  
Vaccine Development ◽  
Mdck Cells ◽  
Influenza Viruses ◽  
Clinical Samples ◽  
Respiratory Epithelial Cells ◽  
Respiratory Epithelial

ABSTRACT Influenza virus isolation from clinical samples is critical for the identification and characterization of circulating and emerging viruses. Yet efficient isolation can be difficult. In these studies, we isolated primary swine nasal and tracheal respiratory epithelial cells and immortalized swine nasal epithelial cells (siNEC) and tracheal epithelial cells (siTEC) that retained the abilities to form tight junctions and cilia and to differentiate at the air-liquid interface like primary cells. Critically, both human and swine influenza viruses replicated in the immortalized cells, which generally yielded higher-titer viral isolates from human and swine nasal swabs, supported the replication of isolates that failed to grow in Madin-Darby canine kidney (MDCK) cells, and resulted in fewer dominating mutations during viral passaging than MDCK cells. IMPORTANCE Robust in vitro culture systems for influenza virus are critically needed. MDCK cells, the most widely used cell line for influenza isolation and propagation, do not adequately model the respiratory tract. Therefore, many clinical isolates, both animal and human, are unable to be isolated and characterized, limiting our understanding of currently circulating influenza viruses. We have developed immortalized swine respiratory epithelial cells that retain the ability to differentiate and can support influenza replication and isolation. These cell lines can be used as additional tools to enhance influenza research and vaccine development.

scholarly journals Influenza virus NS1 protein mutations at position 171 impact innate interferon responses by respiratory epithelial cells

2017 ◽  
Vol 240 ◽  
pp. 81-86 ◽  
Author(s):  
Ewan P. Plant ◽  
Natalia A. Ilyushina ◽  
Faruk Sheikh ◽  
Raymond P. Donnelly ◽  
Zhiping Ye
Keyword(s):  
Influenza Virus ◽  
Epithelial Cells ◽  
Ns1 Protein ◽  
Respiratory Epithelial Cells ◽  
Protein Mutations ◽  
Respiratory Epithelial ◽  
Interferon Responses

scholarly journals Dynamic Virus-Bacterium Interactions in a Porcine Precision-Cut Lung Slice Coinfection Model: Swine Influenza Virus Paves the Way for Streptococcus suis Infection in a Two-Step Process

2015 ◽  
Vol 83 (7) ◽  
pp. 2806-2815 ◽  
Author(s):  
F. Meng ◽  
N. H. Wu ◽  
A. Nerlich ◽  
G. Herrler ◽  
P. Valentin-Weigand ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Epithelial Cells ◽  
Respiratory Tract ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Content Type ◽  
Step Process ◽  
Lung Slice ◽  
Infected Cells ◽  
Ciliated Epithelial Cells

Swine influenza virus (SIV) andStreptococcus suisare common pathogens of the respiratory tract in pigs, with both being associated with pneumonia. The interactions of both pathogens and their contribution to copathogenesis are only poorly understood. In the present study, we established a porcine precision-cut lung slice (PCLS) coinfection model and analyzed the effects of a primary SIV infection on secondary infection byS. suisat different time points. We found that SIV promoted adherence, colonization, and invasion ofS. suisin a two-step process. First, in the initial stages, these effects were dependent on bacterial encapsulation, as shown by selective adherence of encapsulated, but not unencapsulated,S. suisto SIV-infected cells. Second, at a later stage of infection, SIV promotedS. suisadherence and invasion of deeper tissues by damaging ciliated epithelial cells. This effect was seen with a highly virulent SIV subtype H3N2 strain but not with a low-virulence subtype H1N1 strain, and it was independent of the bacterial capsule, since an unencapsulatedS. suismutant behaved in a way similar to that of the encapsulated wild-type strain. In conclusion, the PCLS coinfection model established here revealed novel insights into the dynamic interactions between SIV andS. suisduring infection of the respiratory tract. It showed that at least two different mechanisms contribute to the beneficial effects of SIV forS. suis, including capsule-mediated bacterial attachment to SIV-infected cells and capsule-independent effects involving virus-mediated damage of ciliated epithelial cells.

scholarly journals Influenza A Virus Infection Triggers Pyroptosis and Apoptosis of Respiratory Epithelial Cells through the Type I Interferon Signaling Pathway in a Mutually Exclusive Manner

2018 ◽  
Vol 92 (14) ◽  
Author(s):  
SangJoon Lee ◽  
Mikako Hirohama ◽  
Masayuki Noguchi ◽  
Kyosuke Nagata ◽  
Atsushi Kawaguchi
Keyword(s):  
Cell Death ◽  
Influenza Virus ◽  
Epithelial Cells ◽  
Virus Infection ◽  
Signaling Pathway ◽  
Influenza Virus Infection ◽  
Type I ◽  
Respiratory Epithelial Cells ◽  
Respiratory Epithelial ◽  
Early Phases

ABSTRACT Respiratory epithelial cell death by influenza virus infection is responsible for the induction of inflammatory responses, but the exact cell death mechanism is not understood. Here we showed that influenza virus infection induces apoptosis and pyroptosis in normal or precancerous human bronchial epithelial cells. Apoptosis was induced only in malignant tumor cells infected with influenza virus. In human precancerous respiratory epithelial cells (PL16T), the number of apoptotic cells increased at early phases of infection, but pyroptotic cells were observed at late phases of infection. These findings suggest that apoptosis is induced at early phases of infection but the cell death pathway is shifted to pyroptosis at late phases of infection. We also found that the type I interferon (IFN)-mediated JAK-STAT signaling pathway promotes the switch from apoptosis to pyroptosis by inhibiting apoptosis possibly through the induced expression of the Bcl-xL anti-apoptotic gene. Further, the inhibition of JAK-STAT signaling repressed pyroptosis but enhanced apoptosis in infected PL16T cells. Collectively, we propose that type I IFN signaling pathway triggers pyroptosis but not apoptosis in the respiratory epithelial cells in a mutually exclusive manner to initiate proinflammatory responses against influenza virus infection. IMPORTANCE Respiratory epithelium functions as a sensor of infectious agents to initiate inflammatory responses along with cell death. However, the exact cell death mechanism responsible for inflammatory responses by influenza virus infection is still unclear. We showed that influenza virus infection induced apoptosis and pyroptosis in normal or precancerous human bronchial epithelial cells. Apoptosis was induced at early phases of infection, but the cell death pathway was shifted to pyroptosis at late phases of infection under the regulation of type I IFN signaling to promote proinflammatory cytokine production. Taken together, our results indicate that the type I IFN signaling pathway plays an important role to induce pyroptosis but represses apoptosis in the respiratory epithelial cells to initiate proinflammatory responses against influenza virus infection.

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