Vascular endothelial growth factor–mediated induction of angiogenesis by human rhinoviruses

Psarras, Stelios; Volonaki, Eleni; Skevaki, Chrysanthi; Xatzipsalti, Maria; Bossios, Apostolos; Pratsinis, Harris; Tsigkos, Stelios; Gourgiotis, Dimitrios; Constantopoulos, A; Papapetropoulos, Andreas; Saxoni-Papageorgiou, Photini; Papadopoulos, Nikolaos G.

doi:10.1016/j.jaci.2005.11.005

Cited by 83 publications

(88 citation statements)

References 41 publications

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“…CCL5 is the dominant chemoattractant present in HRV-15 CM, although CXCL8 may also contribute. These data, together with earlier reports that HRV infected epithelial cells show expression of genes related to airway remodeling (33), and release a number of growth factors and matrix proteins linked to airway remodeling (34)(35)(36), further support the concept that recurrent HRV infections may contribute to the initiation and progression of airway remodeling in asthma. Future studies will need to determine if the current observations are relevant to cells obtained from asthmatic subjects (both children and adults), while clinical studies of either naturally-acquired or experimental HRV infections will confirm whether these observations occur in vivo.…”

Section: Hrv-induced Asmc Migration Is Mediated At Least In Part VIsupporting

confidence: 80%

Human Rhinovirus Infection of Epithelial Cells Modulates Airway Smooth Muscle Migration

Shariff

Shelfoon

Holden

et al. 2017

Am J Respir Cell Mol Biol

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Rationale: Airway remodeling, a characteristic feature of asthma, begins in early life. Recurrent human rhinovirus (HRV) infections are a potential inciting stimulus for remodeling. One component of airway remodeling is an increase in airway smooth muscle cell mass with a greater proximity of the airway smooth muscle cells (ASMC) to the airway epithelium. We asked whether human bronchial epithelial cells infected with HRV produced mediators that are chemotactic for ASMC.Methods: ASMC migration was investigated using the modified Boyden Chamber and the xCELLigence Real-Time Cell Analyzer. Multiplex bead analysis was used to measure HRVinduced epithelial chemokine release. The chemotactic effects of CCL5, CXCL8 and CXCL10 were also examined.Results: Supernatants from HRV-infected epithelial cells caused ASMC chemotaxis. Pretreatment of ASMC with pertussis toxin abrogated chemotaxis, as did treatment with formoterol, forskolin, or 8-bromo-cAMP. CCL5, CXCL8, and CXCL10 were most up-regulated chemokines produced by HRV-infected airway epithelial cells. When recombinant CCL5, CXCL8 and CXCL10 were used at levels found in epithelial supernatants they induced ASMC chemotaxis similar to that seen with epithelial cell supernatants. When examined individually, CCL5 was the most effective chemokine in causing ASMC migration and treatment of supernatant from HRVinfected epithelial cells with anti-CCL5 antibodies significantly attenuated ASMC migration. Conclusion:These findings suggest that HRV-induced CCL5 can induce ASMC chemotaxis, and thus may contribute to the pathogenesis of airway remodeling in asthmatic patients.3

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Section: Hrv-induced Asmc Migration Is Mediated At Least In Part VIsupporting

confidence: 80%

Human Rhinovirus Infection of Epithelial Cells Modulates Airway Smooth Muscle Migration

Shariff

Shelfoon

Holden

et al. 2017

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

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“…From another perspective, RV infection has been shown to promote endothelial cell proliferation and differentiation though induction of angiogenetic factors, such as vascular endothelial growth factor (VEGF), possibly contributing to airway remodelling in asthma; this response was further augmented in an atopic host environment [92]. Similar responses were observed for other profibrotic factors, such as transforming growth factor-b [90] and fibroblast growth factor 2 [93].…”

Section: Mechanisms Of Virus-induced Exacerbationmentioning

confidence: 98%

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Xepapadaki¹,

Papadopoulos²

2010

Eur Respir J

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Respiratory infections have been implicated in the origin and exacerbation of asthma in a variety of ways; however, systemisation of this knowledge in a way helpful for disease management remains suboptimal.Several conceptual issues need to be taken into account: the fact that the effects of an infection may vary according to genetic background, the current immune status of the host, and parallel environmental stimuli, in addition to the particular infectious agent itself. Moreover, childhood is a very special period because of the continuous processes taking place, such as neural, immune and respiratory maturation.Epidemiological studies have convincingly demonstrated that the majority of asthma exacerbations, in both adults and children, follow viral upper respiratory tract infections. Asthma exacerbations are still often unresponsive to current asthma treatment, and new therapeutic approaches are required.This review presents current knowledge on the associations between infection and exacerbation of established asthma with respect to definitions, epidemiology, mechanisms and treatment.

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“…The volume and surface densities of the cavernous blood vessels in rhinitis were unaltered and there was no evidence of vascular remodeling. On the other hand, the hypervascularity and overexpression of the platelet-derived endothelial cell growth factor and Vascular Endothelial Growth Factor (VEGF), an angiogenic factor, were found in allergic nasal mucosa (824,825).…”

Section: Allergic Inflammationmentioning

confidence: 99%

Allergic Rhinitis and its Impact on Asthma (ARIA) 2008*

Bousquet¹,

Khaltaev²,

Cruz³

et al. 2008

Allergy

3,859

1,761

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Vascular endothelial growth factor–mediated induction of angiogenesis by human rhinoviruses

Cited by 83 publications

References 41 publications

Human Rhinovirus Infection of Epithelial Cells Modulates Airway Smooth Muscle Migration

Human Rhinovirus Infection of Epithelial Cells Modulates Airway Smooth Muscle Migration

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Allergic Rhinitis and its Impact on Asthma (ARIA) 2008*

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