Human parainfluenza virus serotypes differ in their kinetics of replication and cytokine secretion in human tracheobronchial airway epithelium

Schaap-Nutt, Anne; Liesman, Rachael M.; Bartlett, Emmalene J.; Scull, Margaret A.; Collins, Peter L.; Pickles, Raymond J.; Schmidt, Alexander

doi:10.1016/j.virol.2012.08.027

Cited by 22 publications

(32 citation statements)

References 65 publications

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“…For example, PIV1 infection and growth kinetics in human ciliated cells of HAE was highly reproducible both between cultures derived from an individual donor and HAE derived from 5 different donors (Bartlett et al 2008a, b). Similar data were obtained for influenza viruses (Scull et al 2009) and PIV2 (Schaap-Nutt et al 2012). However, in our experience, not all experimental outcomes are as consistent between donors.…”

Section: Variability Of Virus Infection In Hae Derived From Differentsupporting

confidence: 83%

Human Airway Epithelial Cell Cultures for Modeling Respiratory Syncytial Virus Infection

Pickles

2013

Current Topics in Microbiology and Immunology

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Respiratory syncytial virus (RSV) is an important human respiratory pathogen with narrow species tropism. Limited availability of human pathologic specimens during early RSV-induced lung disease and ethical restrictions for RSV challenge studies in the lower airways of human volunteers has slowed our understanding of how RSV causes airway disease and greatly limited the development of therapeutic strategies for reducing RSV disease burden. Our current knowledge of RSV infection and pathology is largely based on in vitro studies using nonpolarized epithelial cell-lines grown on plastic or in vivo studies using animal models semipermissive for RSV infection. Although these models have revealed important aspects of RSV infection, replication, and associated inflammatory responses, these models do not broadly recapitulate the early interactions and potential consequences of RSV infection of the human columnar airway epithelium in vivo. In this chapter, the pro et contra of in vitro models of human columnar airway epithelium and their usefulness in respiratory virus pathogenesis and vaccine development studies will be discussed. The use of such culture models to predict characteristics of RSV infection and the correlation of these findings to the human in vivo situation will likely accelerate our understanding of RSV pathogenesis potentially identifying novel strategies for limiting the severity of RSV-associated airway disease.

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Section: Variability Of Virus Infection In Hae Derived From Differentsupporting

confidence: 83%

Human Airway Epithelial Cell Cultures for Modeling Respiratory Syncytial Virus Infection

Pickles

2013

Current Topics in Microbiology and Immunology

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“…The induction of high RANTES levels in PIV3 infected of upper airway epithelial cells is consistent with other studies on bronchial epithelial cell monolayers infected with HPIVs and other viruses from Paramyxoviridae family [15,30,31]. In human ciliated airway epithelium infected with PIV3 RANTES concentrations increased gradually from day 2 through day 5 post infection [15]. Increased RANTES secretion was also found after RSV infection in bronchial epithelial cells [30,31] and elevated RANTES levels were reported in nasopharyngeal secretions from RSV-positive children [32].…”

Section: Discussionsupporting

confidence: 91%

“…This is the first study documenting in vitro infection of human nasal epithelial cells (RPMI 2650 line) with HPIV3, and its association with the release of cytokines; in all previous studies only HPIV infections of lower airway epithelium have been examined [15,16,39]. In our model HNECs infected with HPIV3 did not show apparent cytopathology for up to 92 h after infection, and cells viability was not changed up to 48 h, and at 72 h only with the highest virus titres was significantly decreased.…”

Section: Discussionmentioning

confidence: 99%

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Human parainfluenza virus type 3 (HPIV3) induces production of IFNγ and RANTES in human nasal epithelial cells (HNECs)

et al. 2015

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BackgroundHuman parainfluenza virus type 3 (HPIV3), while infecting lower airway epithelial cells induces pneumonia and bronchiolitis in infants and children, and may lead to asthma exacerbations in children and adults. Respiratory viruses invading the airway epithelium activate innate immune response and induce inflammatory cytokine release contributing to the pathophysiology of upper and lower airway disorders. However, the effects of HPIV3 infection on nasal epithelial cells have not been well defined.The aim of this study was to evaluate the effect of the HPIV3 infection on cultured human nasal epithelial cells (HNECs) and the release of interferon gamma and other cytokines.MethodsRPMI 2650, a human nasal epithelial cell line was cultured into confluence and was infected with HPIV3 (MOI of 0.1, 0.01 and 0.001). The protein release into supernatants and mRNA expression of selected cytokines were assessed 24, 48 and 72 h after infection. Cytokine concentrations in supernatants were measured by ELISA and expression of cytokine mRNA in RPMI 2650 cells confirmed by real time RT-PCR analysis.ResultsHNECs infection with HPIV3 did not induce cytotoxicity for at least 48 hours, but significantly increased IFN-γ protein concentration in the cell supernatants at 24 h and 48 h post infection (by 387% and 485% respectively as compared to mock infected cells). At 24 h a significant increase in expression of mRNA for IFNγ was observed. RANTES protein concentration and mRNA expression were significantly increased at 72 h after infection (mean protein concentration: 3.5 ± 1.4 pg/mL for 0.001 MOI, 10.8 ± 4.6 pg/mL for 0.01 MOI and 61.5 ± 18.4 pg/mL for 0.1 MOI as compared to 2.4 ± 1.3 pg/mL for uninfected cells). No measurable concentrations of TNF-α, IL-10, TSLP, IL-8, GM-CSF or eotaxin, were detected in virus infected cells supernatants.ConclusionsHPIV3 effectively infects upper airway epithelial cells and the infection is associated with induction of IFN-γ and generation of RANTES.

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“…In this study, there were statistically significant changes in levels of IL-1Ra, CCL2, and CXCL10, which are mainly produced by monocytes/macrophages and respiratory epithelial cells. The increased production of these cytokines may be related to changes in the ratios of lymphocytes and monocytes during the initial stage of the acute phase of disease (13,14).…”

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confidence: 99%

Alteration in Serum Levels of Inflammatory Cytokines during Parainfluenza Virus Type 1 Infection in Patients with Severe Multiple Disabilities

Matsuda

Kiyota²,

Yoshizumi

et al. 2014

Jpn J Infect Dis

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SUMMARY: An epidemic of parainfluenza virus type 1 (PIV1) infection occurred in a hospital ward housing patients with severe motor and intellectual disabilities. Twenty-three infected patients exhibited persistent high fever for 4-16 days and decreased lymphocyte counts. One-half of the symptomatic patients had increased blood monocyte counts and the other half progressed to bronchitis or pneumonia. We also compared levels of 27 cytokines in the sera of 21 patients during the acute and normal phases of infection. Cytokine levels were measured with a bead immunoassay performed using the Luminex Multiplex System. Serum levels of interleukin (IL)-1Ra, C-C-motif chemokine (CCL) 2, and C-X-C-motif chemokine (CXCL) 10 significantly increased during the acute phase. In contrast, the serum level of CXCL8 decreased slightly. These results suggest the involvement of monocytes/macrophages and respiratory epithelial cells in the initial stage of PIV1 infection. A previous report using nasal wash samples also found a significant increase in levels of CXCL10 during the acute phase. Hence, CXCL10 may be a useful marker of a cytokine storm produced upon viral infection. However, alterations in levels of IL-1Ra, CCL2, and other cytokines differed between the 2 studies, suggesting that the cytokine profile produced systemically at viral infection is different from that produced at mucosal sites. Further analysis is required to clarify the mechanisms underlying cytokine production during PIV1 infections.Human parainfluenza virus (PIV) is commonly identified as a causative agent of respiratory tract infections (1). Among the 4 types of PIV, types 1 (PIV1) and 3 belong to the genus Respirovirus, and types 2 and 4 belong to the genus Rubulavirus. Reportedly, PIV1 and 3 cause infections mainly in the lower respiratory tract, whereas PIV2 and 4 mainly infect the upper respiratory tract. In particular, PIV1 frequently infects epithelial cells of the respiratory tract and induces lower respiratory tract infections, such as bronchitis and pneumonia, especially in immunocompromised hosts, children, and the elderly (1,2).Severe viral infections are known to induce cytokine storms, which impact the progression of infectious diseases (3). During a cytokine storm, interferons (IFNs), interleukins (ILs), chemokines, colony-stimulating factors (CSFs), and tumor necrosis factors (TNFs) are produced in varying amounts, resulting in various immune responses. In addition, infections by the same virus have been reported to induce cytokine storms with different cytokine profiles (2,4). Therefore, specific cytokine responses to individual infectious disease remain under investigation.Here, we report an epidemic of PIV1 infection that occurred in a hospital ward housing patients with severe multiple disabilities. We analyzed the clinical characteristics of PIV1 infection and changes in serum levels of cytokines in symptomatic patients.In a 60-bed ward at Ehime Medical Center (Ehime, Japan), 23 patients (14 men and 9 women) aged 18-68 years (average age,...

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Human parainfluenza virus serotypes differ in their kinetics of replication and cytokine secretion in human tracheobronchial airway epithelium

Cited by 22 publications

References 65 publications

Human Airway Epithelial Cell Cultures for Modeling Respiratory Syncytial Virus Infection

Human Airway Epithelial Cell Cultures for Modeling Respiratory Syncytial Virus Infection

Human parainfluenza virus type 3 (HPIV3) induces production of IFNγ and RANTES in human nasal epithelial cells (HNECs)

Alteration in Serum Levels of Inflammatory Cytokines during Parainfluenza Virus Type 1 Infection in Patients with Severe Multiple Disabilities

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