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3 results on '"Michele, Kong"'

1. Respiratory Syncytial Virus Infection Disrupts Monolayer Integrity and Function in Cystic Fibrosis Airway Cells

Author

Wayne Sullender, John Paul Clancy, Rhonda Szczesniak, Eric Sorscher, Jeong Hong, Patrick Maeng, and Michele Kong

Subjects
Respiratory Syncytial Virus, bronchial epithelial cells, cystic fibrosis, F508del cystic fibrosis transmembrane conductance regulator (CFTR), Microbiology, QR1-502
Abstract

Background: Respiratory Syncytial Virus (RSV) infection is a common contributor to pulmonary symptoms in children with cystic fibrosis (CF). Here we examined RSV infection in immortalized bronchial epithelial cells (CFBE41o-) expressing wild-type (wt) or F508del cystic fibrosis transmembrane conductance regulator (CFTR), for monolayer integrity and RSV replication. Methods: CFBE41o- monolayers expressing wt or F508del CFTR were grown on permeable supports and inoculated with RSV A2 strain. Control experiments utilized UV-inactivated RSV and heat-killed RSV. Monolayer resistance and RSV production was monitored for up to six days post-infection. Results: Within 24 h, a progressive decrease in monolayer resistance was observed in RSV infected F508del CFBE41o- cells, while the monolayer integrity of RSV infected wt CFTR CFBE41o- cells remained stable. RSV replication was necessary to disrupt F508del CFBE41o- monolayers as UV-irradiated and heat killed RSV had no effect on monolayer integrity, with an earlier and much more pronounced peak in RSV titer noted in F508del relative to wt CFTR-expressing cells. RSV infection of wt CFBE41o- monolayers also resulted in blunting of CFTR response. Conclusions: These findings identify an enhanced sensitivity of CFBE41o- cells expressing F508del CFTR to RSV infection, replication and monolayer disruption independent of the cellular immune response, and provide a novel mechanism by which cystic fibrosis airway epithelia are susceptible to RSV-dependent injury.

Published
2013
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2. Matrix Metalloproteinase-9 Mediates RSV Infection in Vitro and in Vivo

Author

Wayne M. Sullender, Ning Peng, John P. Clancy, Robert A. Oster, Namasivayam Ambalavanan, Trenton R. Schoeb, Amit Gaggar, J. Edwin Blalock, Michele Kong, and Richard J. Whitley

Subjects
matrix metalloproteinase, viruses, respiratory syncytial virus, lcsh:QR1-502, Inflammation, cell, murine model, Transfection, Biology, respiratory system, Virology, Virus, In vitro, lcsh:Microbiology, Article, Infectious Diseases, Viral replication, In vivo, medicine, Gene silencing, medicine.symptom, Viral load
Abstract

Respiratory Syncytial Virus (RSV) is an important human pathogen associated with substantial morbidity and mortality. The present study tested the hypothesis that RSV infection would increase matrix metalloproteinase (MMP)-9 expression, and that MMP-9 inhibition would decrease RSV replication both in vitro and in vivo. RSV A2 infection of human bronchial epithelial cells increased MMP-9 mRNA and protein release. Cells transfected with siRNA against MMP-9 following RSV infection had lower viral titers. In RSV infected wild-type (WT) mice, MMP-9, airway resistance and viral load peaked at day 2 post infection, and remained elevated on days 4 and 7. RSV infected MMP-9 knockout (KO) mice had decreased lung inflammation. On days 2 and 4 post inoculation, the RSV burden was lower in the MMP-9 KO mice compared to WT controls. In conclusion, our studies demonstrate that RSV infection is a potent stimulus of MMP-9 expression both in vitro and in vivo. Reduction of MMP-9 (via siRNA knockdown, and in MMP-9 KO mice) resulted in decreased viral replication. Our findings suggest MMP-9 is a potential therapeutic target for RSV disease.

Published
2015
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3. Addendum: Kong, M.Y.; Whitley, R.J.; Peng, N.; Oster, R.; Schoeb, T.R.; Sullender, W.; Ambalavanan, N.; Clancy, J.P.; Gaggar, A.; Blalock J.E. Matrix Metalloproteinase-9 Mediates RSV Infection in Vitro and in Vivo. Viruses 2015, 30, 7, 4230–4253

Author

J.E. Blalock, Ning Peng, Robert A. Oster, Trenton R. Schoeb, Namasivayam Ambalavanan, Amit Gaggar, Wayne M. Sullender, John P. Clancy, Richard J. Whitley, and Michele Kong

Subjects
Smoking prevention, lcsh:QR1-502, Bioinformatics, lcsh:Microbiology, Virology, Medicine, Animals, Humans, Gene Silencing, RNA, Small Interfering, Lung, Cells, Cultured, Mice, Knockout, business.industry, Addendum, Matrix metalloproteinase 9, Epithelial Cells, Viral Load, 3. Good health, Respiratory Syncytial Viruses, Mice, Inbred C57BL, Infectious Diseases, n/a, Matrix Metalloproteinase 9, Host-Pathogen Interactions, business
Abstract

Respiratory Syncytial Virus (RSV) is an important human pathogen associated with substantial morbidity and mortality. The present study tested the hypothesis that RSV infection would increase matrix metalloproteinase (MMP)-9 expression, and that MMP-9 inhibition would decrease RSV replication both in vitro and in vivo. RSV A2 infection of human bronchial epithelial cells increased MMP-9 mRNA and protein release. Cells transfected with siRNA against MMP-9 following RSV infection had lower viral titers. In RSV infected wild-type (WT) mice, MMP-9, airway resistance and viral load peaked at day 2 post infection, and remained elevated on days 4 and 7. RSV infected MMP-9 knockout (KO) mice had decreased lung inflammation. On days 2 and 4 post inoculation, the RSV burden was lower in the MMP-9 KO mice compared to WT controls. In conclusion, our studies demonstrate that RSV infection is a potent stimulus of MMP-9 expression both in vitro and in vivo. Reduction of MMP-9 (via siRNA knockdown, and in MMP-9 KO mice) resulted in decreased viral replication. Our findings suggest MMP-9 is a potential therapeutic target for RSV disease.

Published
2015

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