In vitro susceptibility to rhinovirus infection is greater for bronchial than for nasal airway epithelial cells in human subjects

Lopez-Souza, Nilceia; Favoreto, Sílvio; Wong, Hofer; Ward, Theresa A.; Yagi, Shigeo; Schnurr, David P.; Finkbeiner, Walter E.; Dolganov, Gregory; Widdicombe, Jonathan; Boushey, Homer A.; Avila, Pedro C.

doi:10.1016/j.jaci.2009.03.010

Cited by 182 publications

(161 citation statements)

References 39 publications

Supporting

Mentioning

147

Contrasting

Order By: Relevance

“…Looking at the absolute values in the controls in our study, the bronchial epithelial cells produced the smallest amounts of IL-6 protein. This is consistent with previously published results [26,34]. Stimulation with TNF-α resulted in a greater increase in the IL-6 level in bronchial cells.…”

Section: Discussionsupporting

confidence: 94%

The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

Paplińska-Goryca

Nejman-Gryz

Chazan

et al. 2013

Cellular and Molecular Biology Letters

View full text Add to dashboard Cite

Airway epithelium acts as multifunctional site of response in the respiratory tract. Epithelial activity plays an important part in the pathophysiology of obstructive lung disease. In this study, we compare normal human epithelial cells from various levels of the respiratory tract in terms of their reactivity to pro-allergic and pro-inflammatory stimulation. Normal human nasal, bronchial and small airway epithelial cells were stimulated with IL-4 and IL-13. The expressions of the eotaxins IL-6 and CXCL8 were evaluated at the mRNA and protein levels. The effects of pre-treatment with IFN-γ on the cell reactivity were measured, and the responses to TNF-α, LPS and IFN-γ were evaluated. All of the studied primary cells expressed CCL26, IL-6 and IL-8 after IL-4 or IL-13 stimulation. IFN-γ pre-treatment resulted in decreased CCL26 and increased IL-6 expression in the nasal and small airway cells, but this effect was not observed in the bronchial cells. IL-6 and CXCL8 were produced in varying degrees by all of the epithelial primary cells in cultures stimulated with TNF-α, LPS or IFN-γ. We showed that epithelial cells from the various levels of the respiratory tract act in a united way, responding in a similar manner to stimulation with IL-4 and IL-13, showing similar reactivity to TNF-α and LPS, and giving an almost unified response to IFN-γ pre-stimulation.

show abstract

Section: Discussionsupporting

confidence: 94%

The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

Paplińska-Goryca

Nejman-Gryz

Chazan

et al. 2013

Cellular and Molecular Biology Letters

View full text Add to dashboard Cite

show abstract

“…It also allows investigation of patients with severe or uncontrolled asthma phenotypes without stopping their long-term inhaled corticosteroid treatment for asthma, as nasal deposition can be considered as negligible with the devices used in this study [22]. Interestingly, we observed a good overlap between our ''nasal epithelial'' gene lists and several gene expression profiles in bronchial epithelium, notwithstanding differences between nasal and bronchial epithelial cells [23,24], such as the near absence of remodelling in the nasal epithelium [25]. In this context, the use of alternative techniques to harvest lower airway cells during general anaesthesia could be worth investigating [26].…”

Section: Discussionmentioning

confidence: 74%

Distinct epithelial gene expression phenotypes in childhood respiratory allergy

Giovannini‐Chami¹,

Marcet²,

Moreilhon³

et al. 2011

Eur Respir J

View full text Add to dashboard Cite

Epithelial cell contribution to the natural history of childhood allergic respiratory disease remains poorly understood. Our aims were to identify epithelial pathways that are dysregulated in different phenotypes of respiratory allergy.We established gene expression signatures of nasal brushings from children with dust miteallergic rhinitis, associated or not associated with controlled or uncontrolled asthma. Supervised learning and unsupervised clustering were used to predict the different subgroups of patients and define altered signalling pathways. These profiles were compared with those of primary cultures of human nasal epithelial cells stimulated with either interleukin (IL)-4, IL-13, interferon (IFN)-a, IFN-b or IFN-c, or during in vitro differentiation.A supervised method discriminated children with allergic rhinitis from healthy controls (prediction accuracy 91%), based on 61 transcripts, including 21 T-helper cell (Th) type 2-responsive genes. This method was then applied to predict children with controlled or uncontrolled asthma (prediction accuracy 75%), based on 41 transcripts: nine of them, which were down-regulated in uncontrolled asthma, are directly linked to IFN. This group also included GSDML, which is genetically associated with asthma.Our data revealed a Th2-driven epithelial phenotype common to all children with dust mite allergic rhinitis. It highlights the influence of epithelially expressed molecules on the control of asthma, in association with atopy and impaired viral response.

show abstract

“…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.

170

217

View full text Add to dashboard Cite

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.

show abstract

In vitro susceptibility to rhinovirus infection is greater for bronchial than for nasal airway epithelial cells in human subjects

Abstract: Background-Human rhinoviruses (HRVs) characteristically cause upper respiratory tract infection but they also infect the lower airways causing acute bronchitis and exacerbating asthma.

Cited by 182 publications

References 39 publications

The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

Distinct epithelial gene expression phenotypes in childhood respiratory allergy

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

Contact Info

Product

Resources

About