scholarly journals The Role of Trypsin in The Internalization Process of Influenza H1N1 Virus into Vero and MDCK Cells

2012 ◽  
Vol 44 (4) ◽  
pp. 297-307 ◽  
Author(s):  
Fawzi Rahmadiyan Zuhairi ◽  
◽  
Maharani Maharani ◽  
Marselina I. Tan ◽  
Keyword(s):  
H1n1 Virus ◽  
Mdck Cells ◽  
Internalization Process ◽  
Influenza H1n1

scholarly journals Host DNA released by NETosis in neutrophils exposed to seasonal H1N1 and highly pathogenic H5N1 influenza viruses

2020 ◽  
Author(s):  
Louisa L.Y. Chan ◽  
John M. Nicholls ◽  
J.S. Malik Peiris ◽  
Yu Lung Lau ◽  
Michael C.W. Chan ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
H1n1 Virus ◽  
Influenza Virus Infection ◽  
Alveolar Epithelium ◽  
Influenza Viruses ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza ◽  
Influenza H1n1

Abstract Background Neutrophil (Nϕ) is of the most abundant number in human immune system. During acute influenza virus infection, Nϕs are already active in the early phase of inflammation-a time in which clinical biopsy or autopsy material is not readily available. However, the role of Nϕ in virus infection is not well understood. Here, we studied the role of Nϕ in host defense during influenza A virus infection, specifically assessing if it contributes to the differential pathogenesis in H5N1 disease. Methods Nϕs were freshly isolated from healthy volunteers and subjected to direct influenza H1N1 and H5N1 virus infection in vitro . The ability of the naïve Nϕs to infiltrate from the basolateral to the apical phase of the influenza virus infected alveolar epithelium was assessed. The viral replication, innate immune responses and Neutrophil extracellular trap (NET) formation of Nϕs upon influenza virus infection were evaluated. Results Our results demonstrated that influenza virus infected alveolar epithelium allowed more Nϕs transmigration. Significantly more Nϕs migrated across the H5N1 influenza virus infected the epithelium than the counterpart infected by the seasonal influenza H1N1 virus infected. Nϕs were equally susceptible to H5N1 and H1N1 virus infection with similar viral gene transcription. Productive replication was observed in H5N1 infected Nϕs. Both H5N1 and H1N1 infected Nϕs induced cytokines and chemokines including TNF-α, IFN-β, CXCL10, MIP-1α and IL-8. This inferred a more intense inflammatory response posed by H5N1 than H1N1 virus. Strikingly, NADPH oxidase-independent NET formation was observed in H1N1 infected Nϕs at 6 hpi while no NET formation was observed upon H5N1 infection. Conclusion Our data is the first to demonstrate that NET formation is abrogated in H5N1 influenza virus infection. Its contribution to the differential severity of H5N1 disease requires further investigation.

scholarly journals Host DNA released by NETosis in neutrophils exposed to seasonal H1N1 and highly pathogenic H5N1 influenza viruses

2020 ◽  
Author(s):  
Louisa L.Y. Chan ◽  
John M. Nicholls ◽  
J.S. Malik Peiris ◽  
Yu Lung Lau ◽  
Michael C.W. Chan ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Gene Transcription ◽  
H1n1 Virus ◽  
Influenza Virus Infection ◽  
Alveolar Epithelium ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza ◽  
Influenza H1n1

Abstract Background: Neutrophil is of the most abundant number in human immune system. During acute influenza virus infection, neutrophils are already active in the early phase of inflammation-a time in which clinical biopsy or autopsy material is not readily available. However, the role of neutrophil in virus infection is not well understood. Here, we studied the role of neutrophil in host defense during influenza A virus infection, specifically assessing if it contributes to the differential pathogenesis in H5N1 disease. Methods: Neutrophils were freshly isolated from healthy volunteers and subjected to direct influenza H1N1 and H5N1 virus infection in vitro. The ability of the naïve neutrophils to infiltrate from the basolateral to the apical phase of the influenza virus infected alveolar epithelium was assessed. The viral replication, innate immune responses and Neutrophil extracellular trap (NET) formation of neutrophils upon influenza virus infection were evaluated. Results: Our results demonstrated that influenza virus infected alveolar epithelium allowed more neutrophils transmigration. Significantly more neutrophils migrated across the H5N1 influenza virus infected the epithelium than the counterpart infected by the seasonal influenza H1N1 virus infected. Neutrophils were equally susceptible to H5N1 and H1N1 virus infection with similar viral gene transcription. Productive replication was observed in H5N1 infected neutrophils. H5N1 induced higher cytokine and chemokine gene transcription than H1N1 infected neutrophils, including TNF-α, IFN-β, CXCL10, MIP-1α and IL-8. This inferred a more intense inflammatory response posed by H5N1 than H1N1 virus. Strikingly, NADPH oxidase-independent NET formation was only observed in H1N1 infected neutrophils at 6 hpi while no NET formation was observed upon H5N1 infection.Conclusion: Our data is the first to demonstrate that NET formation is abrogated in H5N1 influenza virus infection and might contribute to the severity of H5N1 disease.

scholarly journals Host DNA released by NETosis in neutrophils exposed to seasonal H1N1 and highly pathogenic H5N1 influenza viruses

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Louisa L. Y. Chan ◽  
John M. Nicholls ◽  
J. S. Malik Peiris ◽  
Yu Lung Lau ◽  
Michael C. W. Chan ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Gene Transcription ◽  
H1n1 Virus ◽  
Influenza Virus Infection ◽  
Alveolar Epithelium ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza ◽  
Influenza H1n1

Abstract Background Neutrophil is of the most abundant number in human immune system. During acute influenza virus infection, neutrophils are already active in the early phase of inflammation - a time in which clinical biopsy or autopsy material is not readily available. However, the role of neutrophil in virus infection is not well understood. Here, we studied the role of neutrophil in host defense during influenza A virus infection, specifically assessing if it contributes to the differential pathogenesis in H5N1 disease. Methods Neutrophils were freshly isolated from healthy volunteers and subjected to direct influenza H1N1 and H5N1 virus infection in vitro. The ability of the naïve neutrophils to infiltrate from the basolateral to the apical phase of the influenza virus infected alveolar epithelium was assessed. The viral replication, innate immune responses and Neutrophil extracellular trap (NET) formation of neutrophils upon influenza virus infection were evaluated. Results Our results demonstrated that influenza virus infected alveolar epithelium allowed neutrophil transmigration. Significantly more neutrophils migrated across the H5N1 influenza virus infected the epithelium than the counterpart infected by the seasonal influenza H1N1 virus infected. Neutrophils were equally susceptible to H5N1 and H1N1 virus infection with similar viral gene transcription. Productive replication was observed in H5N1 infected neutrophils. H5N1 induced higher cytokine and chemokine gene transcription than H1N1 infected neutrophils, including TNF-α, IFN-β, CXCL10, MIP-1α and IL-8. This inferred a more intense inflammatory response posed by H5N1 than H1N1 virus. Strikingly, NADPH oxidase-independent NET formation was only observed in H1N1 infected neutrophils at 6 hpi while no NET formation was observed upon H5N1 infection. Conclusion Our data is the first to demonstrate that NET formation is abrogated in H5N1 influenza virus infection and might contribute to the severity of H5N1 disease.

scholarly journals Rapid and Efficient Cell-to-Cell Transmission of Avian Influenza H5N1 Virus in MDCK Cells Is Achieved by Trogocytosis

Pathogens ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 483
Author(s):  
Supasek Kongsomros ◽  
Suwimon Manopwisedjaroen ◽  
Jarinya Chaopreecha ◽  
Sheng-Fan Wang ◽  
Suparerk Borwornpinyo ◽  
...  
Keyword(s):  
H5n1 Virus ◽  
H1n1 Virus ◽  
Mdck Cells ◽  
Cell Transfer ◽  
Human Influenza ◽  
Cell Transmission ◽  
Transfer Strategies ◽  
Direct Cell ◽  
Cell To Cell Transfer ◽  
Influenza H1n1

Viruses have developed direct cell-to-cell transfer strategies to enter target cells without being released to escape host immune responses and antiviral treatments. These strategies are more rapid and efficient than transmission through indirect mechanisms of viral infection between cells. Here, we demonstrate that an H5N1 influenza virus can spread via direct cell-to-cell transfer in Madin-Darby canine kidney (MDCK) cells. We compared cell-to-cell transmission of the H5N1 virus to that of a human influenza H1N1 virus. The H5N1 virus has been found to spread to recipient cells faster than the human influenza H1N1 virus. Additionally, we showed that plasma membrane exchange (trogocytosis) occurs between co-cultured infected donor cells and uninfected recipient cells early point, allowing the intercellular transfer of viral material to recipient cells. Notably, the H5N1 virus induced higher trogocytosis levels than the H1N1 virus, which could explain the faster cell-to-cell transmission rate of H5N1. Importantly, this phenomenon was also observed in A549 human lung epithelial cells, which are representative cells in the natural infection site. Altogether, our results provide evidence demonstrating that trogocytosis could be the additional mechanism utilized by the H5N1 virus for rapid and efficient cell-to-cell transmission.

scholarly journals Phosphorylation of Rab11-FIP2 regulates polarity in MDCK cells

2012 ◽  
Vol 23 (12) ◽  
pp. 2302-2318 ◽  
Author(s):  
Lynne A. Lapierre ◽  
Kenya M. Avant ◽  
Cathy M. Caldwell ◽  
Asli Oztan ◽  
Gerard Apodaca ◽  
...  
Keyword(s):  
Tight Junctions ◽  
Mdck Cell ◽  
Mdck Cells ◽  
Adherens Junction ◽  
Cellular Polarity ◽  
Interacting Protein ◽  
P120 Catenin ◽  
Myosin Vb ◽  
Darby Canine Kidney

The Rab11 effector Rab11-family interacting protein 2 (Rab11-FIP2) regulates transcytosis through its interactions with Rab11a and myosin Vb. Previous studies implicated Rab11-FIP2 in the establishment of polarity in Madin–Darby canine kidney (MDCK) cells through phosphorylation of Ser-227 by MARK2. Here we examine the dynamic role of Rab11-FIP2 phosphorylation on MDCK cell polarity. Endogenous Rab11-FIP2 phosphorylated on Ser-227 coalesces on vesicular plaques during the reestablishment of polarity after either monolayer wounding or calcium switch. Whereas expression of the nonphosphorylatable Rab11-FIP2(S227A) elicits a loss in lumen formation in MDCK cell cysts grown in Matrigel, the putative pseudophosphorylated Rab11-FIP2(S227E) mutant induces the formation of cysts with multiple lumens. On permeable filters, Rab11-FIP2(S227E)–expressing cells exhibit alterations in the composition of both the adherens and tight junctions. At the adherens junction, p120 catenin and K-cadherin are retained, whereas the majority of the E-cadherin is lost. Although ZO-1 is retained at the tight junction, occludin is lost and the claudin composition is altered. Of interest, the effects of Rab11-FIP2 on cellular polarity did not involve myosin Vb or Rab11a. These results indicate that Ser-227 phosphorylation of Rab11-FIP2 regulates the composition of both adherens and tight junctions and is intimately involved in the regulation of polarity in epithelial cells.

scholarly journals Preventive Activity against Influenza (H1N1) Virus by Intranasally Delivered RNA-Hydrolyzing Antibody in Respiratory Epithelial Cells of Mice

Viruses ◽  
2015 ◽  
Vol 7 (9) ◽  
pp. 5133-5144 ◽  
Author(s):  
Seungchan Cho ◽  
Ha-Na Youn ◽  
Phuong Hoang ◽  
Sungrae Cho ◽  
Kee-Eun Kim ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
H1n1 Virus ◽  
Respiratory Epithelial Cells ◽  
Preventive Activity ◽  
Respiratory Epithelial ◽  
Influenza H1n1

scholarly journals Role of Mitochondrial Na+ Concentration, Measured by CoroNa Red, in the Protection of Metabolically Inhibited MDCK Cells

2005 ◽  
Vol 16 (12) ◽  
pp. 3490-3497 ◽  
Author(s):  
Szilvia Baron ◽  
Adrian Caplanusi ◽  
Martin van de Ven ◽  
Mihai Radu ◽  
Sanda Despa ◽  
...  
Keyword(s):  
Mdck Cells

scholarly journals Pseudomonas aeruginosa-Mediated Damage Requires Distinct Receptors at the Apical and Basolateral Surfaces of the Polarized Epithelium

2009 ◽  
Vol 78 (3) ◽  
pp. 939-953 ◽  
Author(s):  
Iwona Bucior ◽  
Keith Mostov ◽  
Joanne N. Engel
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Mdck Cells ◽  
Three Dimensional ◽  
Opportunistic Pathogen ◽  
Necessary And Sufficient ◽  
Plastic Surfaces ◽  
Pharmacologic Inhibition ◽  
Increased Susceptibility ◽  
Polarized Epithelium

ABSTRACT Pseudomonas aeruginosa, an important opportunistic pathogen of humans, exploits epithelial damage to establish infection. We have rigorously explored the role of N-glycoproteins and heparan sulfate proteoglycans (HSPGs) in P. aeruginosa-mediated attachment and subsequent downstream events at the apical (AP) and basolateral (BL) surfaces of polarized epithelium. We demonstrate that the N-glycan chains at the AP surface are necessary and sufficient for binding, invasion, and cytotoxicity to kidney (MDCK) and airway (Calu-3) cells grown at various states of polarization on Transwell filters. Upregulation of N-glycosylation enhanced binding, whereas pharmacologic inhibition of N-glycosylation or infection of MDCK cells defective in N-glycosylation resulted in decreased binding. In contrast, at the BL surface, the HS moiety of HSPGs mediated P. aeruginosa binding, cytotoxicity, and invasion. In incompletely polarized epithelium, HSPG abundance was increased at the AP surface, explaining its increased susceptibility to P. aeruginosa colonization and damage. Using MDCK cells grown as three-dimensional cysts as a model for epithelial organs, we show that P. aeruginosa specifically colocalized with HS-rich areas at the BL membrane but with complex N-glycans at the AP surface. Finally, P. aeruginosa bound to HS chains and N-glycans coated on plastic surfaces, showing the highest binding affinity toward isolated HS chains. Together, these findings demonstrate that P. aeruginosa recognizes distinct receptors on the AP and BL surfaces of polarized epithelium. Changes in the composition of N-glycan chains and/or in the distribution of HSPGs may explain the enhanced susceptibility of damaged epithelium to P. aeruginosa.

scholarly journals Docking study of flavonoid derivatives as potent inhibitors of influenza H1N1 virus neuraminidase

2018 ◽  
Author(s):  
Seyed Sadati ◽  
Nematollah Gheibi ◽  
Saeed Ranjbar ◽  
Mohammad Hashemzadeh
Keyword(s):  
H1n1 Virus ◽  
Docking Study ◽  
Influenza H1n1
Sign in / Sign up

Export Citation Format

Share Document