NCI-H292 as an alternative cell line for the isolation and propagation of the human paramyxoviruses

Castells, E.; George, Velma G.; Hierholzer, John C.

doi:10.1007/bf01310536

Cited by 28 publications

(17 citation statements)

References 34 publications

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“…It is report ed that NCI-H292 cells are available for culture of paramy xoviruses and may be sensitive to other viruses, including influenza vims [5]. At 48-72 h after virus inoculation, cyto pathic effects, such as rounding of cells and cellular fusion, were observed in the present study.…”

Section: Discussionsupporting

confidence: 57%

Expression of Cytokines on Human Bronchial Epithelial Cells Induced by Influenza Virus A

Adachi

Matsukura

Tokunaga

et al. 1997

Int Arch Allergy Immunol

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Bronchial epithelial cells play an important role in the pathogenesis of some inflammatory diseases of bronchial mucosa. Epithelial-cell-derived cytokines are important in the elucidation of the mechanism by which airway inflammation occurs, especially in respiratory virus infection, because these cells are the primary sites of viral infection. We infected bronchial epithelial cells, NCI-H292, with influenza virus A (H3N2) and examined the concentrations of cytokines, interleukin-6 (IL-6), IL-8 and regulated on activation, normal T cells, expressed and secreted (RANTES), in the culture media of infected cells using the enzyme-linked immunosorbent assay system and gene expression of RANTES on epithelial cells by the reverse-transcriptase-polymerase chain reaction method. We found that significant amounts of IL-6, IL-8 and RANTES were released. RANTES mRNA was also detected in infected bronchial epithelial cells. It is suggested that cytokine production in human bronchial epithelial cells may contribute to the pathogenesis of airway inflammatory disorders.

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Section: Discussionsupporting

confidence: 57%

Expression of Cytokines on Human Bronchial Epithelial Cells Induced by Influenza Virus A

Adachi

Matsukura

Tokunaga

et al. 1997

Int Arch Allergy Immunol

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“…In the present study we determined the mechanisms for IL-8 and IL-6 induction by parainfluenza virus type 4a (PIV-4). For these studies we employed human lung-derived mucoepidermoid adenocarcinoma NCI-H292 cells, which previously were shown to facilitate replication of PIV-4 without causing marked cytopathic effects (5). Moreover, the regulation of IL-8 and IL-6 production in NCI-H292 cells has been studied in detail (24,28,29,35).…”

mentioning

confidence: 99%

Exaggerated IL-8 and IL-6 responses to TNF-α by parainfluenza virus type 4-infected NCI-H292 cells

Roger¹,

Bresser²,

Snoek³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Respiratory viruses induce and potentiate airway inflammation, which is related to the induction of proinflammatory mediators such as interleukin (IL)-8 and IL-6. Here we report on mechanisms implicated in IL-8 and IL-6 production by airway epithelium-like NCI-H292 cells exposed to parainfluenza virus type 4a (PIV-4). PIV-4 readily infected NCI-H292 cells as reflected by intracellular PIV-4 antigen expression. PIV-4 infection triggered a biphasic IL-8 and IL-6 mRNA response. Transient transfection with truncated and mutated promoter constructs identified NF-κB and activator protein (AP)-1, and CCAAT-enhancer binding protein (C/EBP) as the relevant transcription factors for PIV-4-induced IL-8 and IL-6 gene transcription, respectively. An increase of DNA-binding activities for NF-κB and C/EBP paralleled the induction of the first and second IL-8 and IL-6 mRNA peaks, whereas the onset of AP-1 paralleled the first IL-8 mRNA peak only. The second mRNA peak, apparently dependent on viral replication, coincided also with a marked reduction of IL-8 and IL-6 mRNA degradation. Importantly, cells at the time of the reduced mRNA degradation displayed an exaggerated IL-8 and IL-6 protein production to a secondary stimulus, as exemplified by steeper dose-response curves to TNF-α. Thus PIV-4 infection enhances epithelial IL-8 and IL-6 production by transcriptional and posttranscriptional mechanisms. The previously unrecognized phase of reduced IL-8 and IL-6 mRNA degradation and the concurrent amplified epithelial IL-8 and IL-6 responses may play an important role in virus-induced potentiation of airway inflammation.

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“…Les analyses phylogénétiques montrent que, parmi les membres de la sous-famille des Pneumovirinae, le hMPV est étroitement apparenté au sérotype C des pneumovirus aviaires, et qu'il existe des deux sous-groupes de hMPV [5,6]. Elles permettent d'identifier deux sous-groupes majeurs de hMPV et deux sous-groupes mineurs à l'intérieur de chacun d'eux [7][8][9][10]. La souche de référence du hMPV est la souche hollandaise : NETH-001 ; elle appartient au sous-groupe 1 ou A selon les auteurs.…”

Section: Génome Viralunclassified

Métapneumovirus humain

Freymuth

Vabret

Legrand³

et al. 2009

Pathologie Biologie

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The human metapneumovirus (hMPV) is a new Pneumovirinae related to the avian metapneumovirus type C. hMPV genome differs from human respiratory syncytial virus (RSV) genome by the gene order and the lack of nonstructural genes. Two genetic sub-groups and four sub-types of hMPV are identified. hMPV infections evolve as regular winter outbreaks which have roughly the same size and overlaping RSV epidemics. Among hospitalized children in Caen, hMPV is detected in 9.7% of the cases after RSV (37%), rhinovirus (18%), influenza virus (14.5%), adenovirus (9%), and parainfluenza virus (5%). Most of hMPV infections are observed in children suffering from bronchiolitis, but the localization to lower respiratory tract and the severity of the disease are less frequent in comparison with RSV infections. hMPV is very difficult to isolate using cell culture. Up to now, the only way for hMPV diagnosis was the TS-CRP assays. But the recent apparition of direct antigenic tests allows us to get a fair, rapid, and economic diagnostic tool.

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NCI-H292 as an alternative cell line for the isolation and propagation of the human paramyxoviruses

Cited by 28 publications

References 34 publications

Expression of Cytokines on Human Bronchial Epithelial Cells Induced by Influenza Virus A

Expression of Cytokines on Human Bronchial Epithelial Cells Induced by Influenza Virus A

Exaggerated IL-8 and IL-6 responses to TNF-α by parainfluenza virus type 4-infected NCI-H292 cells

Métapneumovirus humain

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