Cytopathogenesis of Sendai Virus in Well-Differentiated Primary Pediatric Bronchial Epithelial Cells

Villenave, Rémi; Touzelet, Olivier; Thavagnanam, Surendran; Sarlang, Séverine; Parker, Jeremy; Skibiński, Grzegorz; Heaney, Liam G.; McKaigue, James P.; Coyle, Peter; Shields, Michael; Power, Ultan F.

doi:10.1128/jvi.00798-10

Cited by 36 publications

(43 citation statements)

References 46 publications

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“…PBECs were obtained from healthy children undergoing elective surgery (n = 5) (42). The generation and characterization of WD-PBEC cultures were described previously and are outlined in SI Materials and Methods (21,43). Briefly, primary cells were expanded in collagen-coated flasks until almost confluent and then were transferred onto collagen-coated semipermeable (0.4-μm pore size, 12-mm diameter) membrane supports.…”

Section: Methodsmentioning

confidence: 99%

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In vitro modeling of respiratory syncytial virus infection of pediatric bronchial epithelium, the primary target of infection in vivo

Villenave

Thavagnanam

Sarlang

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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174

217

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Respiratory syncytial virus (RSV) is the major viral cause of severe pulmonary disease in young infants worldwide. However, the mechanisms by which RSV causes disease in humans remain poorly understood. To help bridge this gap, we developed an ex vivo/in vitro model of RSV infection based on well-differentiated primary pediatric bronchial epithelial cells (WD-PBECs), the primary targets of RSV infection in vivo. Our RSV/WD-PBEC model demonstrated remarkable similarities to hallmarks of RSV infection in infant lungs. These hallmarks included restriction of infection to noncontiguous or small clumps of apical ciliated and occasional nonciliated epithelial cells, apoptosis and sloughing of apical epithelial cells, occasional syncytium formation, goblet cell hyperplasia/metaplasia, and mucus hypersecretion. RSV was shed exclusively from the apical surface at titers consistent with those in airway aspirates from hospitalized infants. Furthermore, secretion of proinflammatory chemokines such as CXCL10, CCL5, IL-6, and CXCL8 reflected those chemokines present in airway aspirates. Interestingly, a recent RSV clinical isolate induced more cytopathogenesis than the prototypic A2 strain. Our findings indicate that this RSV/WD-PBEC model provides an authentic surrogate for RSV infection of airway epithelium in vivo. As such, this model may provide insights into RSV pathogenesis in humans that ultimately lead to successful RSV vaccines or therapeutics.

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Section: Methodsmentioning

confidence: 99%

“…In this regard, the recent advent of technology to culture primary human airway epithelial cells into physiologically authentic pseudostratified airway epithelial (HAE) cultures is very attractive (16). Indeed, such cultures already have been used to study a number of respiratory virus-host interactions, including RSV (17)(18)(19)(20)(21)(22)(23).…”

mentioning

confidence: 99%

In vitro modeling of respiratory syncytial virus infection of pediatric bronchial epithelium, the primary target of infection in vivo

Villenave

Thavagnanam

Sarlang

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

174

217

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show abstract

“…Thus, a large number of viruses may evoke viremia and induce uncontrollable inflammatory reactions. In contrast, the oncolysis that is caused by BioKnife TM is cell death that is mediated by caspase-dependent apoptosis [13,25]. There is no need to worry about viremia, even if an explosive spread of infection is observed.…”

Section: Oncolytic Virotherapy With Sevmentioning

confidence: 99%

“…The fusion process, which occurs between the viral envelope and cells, may also occur between adjacent viral-infected cells when the Fusion protein is expressed on the cell surface, thus causing extensive membrane fusion and the formation of a syncytium. Cell-to-cell fusion induces apoptotic signals, resulting in cell death [12,13].…”

Section: Fusogenic Activity Of Sevmentioning

confidence: 99%

Sendai Virus-Based Oncolytic Gene Therapy

Morodomi¹,

Hasegawa²,

Okamoto³

et al. 2013

Novel Gene Therapy Approaches

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“…However, it is possible that loosely adherent syncytia were washed off the apical surface in collection of supernatants for viral titration. Sendai virus (a paramyxovirus) readily causes syncytia in an elegant HAE system of well-differentiated pediatric bronchial epithelial cells (WD-PBEC) (Villenave et al, 2010). In non-polarized monolayers of primary pediatric bronchial epithelial cells, HRSV A2 replicated to higher titers and caused greater CPE than HRSV clinical isolates (Villenave et al, 2011).…”

Section: Primary Cell Culture Models Of Hrsv Infectionmentioning

confidence: 99%

Animal Models of Respiratory Syncytial Virus Pathogenesis and Vaccine Development: Opportunities and Future Directions

Woolums¹,

Moore²

2011

Human Respiratory Syncytial Virus Infection

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Cytopathogenesis of Sendai Virus in Well-Differentiated Primary Pediatric Bronchial Epithelial Cells

Cited by 36 publications

References 46 publications

In vitro modeling of respiratory syncytial virus infection of pediatric bronchial epithelium, the primary target of infection in vivo

In vitro modeling of respiratory syncytial virus infection of pediatric bronchial epithelium, the primary target of infection in vivo

Sendai Virus-Based Oncolytic Gene Therapy

Animal Models of Respiratory Syncytial Virus Pathogenesis and Vaccine Development: Opportunities and Future Directions

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