Eosinophil activation and cysteinyl leukotriene production in infants with respiratory syncytial virus bronchiolitis

Dimova-Yaneva, D.; Russell, Daphne; Main, Margaret Jessie Campbell; Brooker, Richard; Helms, Peter Joseph Benedict

doi:10.1111/j.1365-2222.2004.1918.x

Cited by 60 publications

(50 citation statements)

References 34 publications

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“…Cys-LTs are potent bronchoconstrictors, as well as proinflammatory mediators, and their role in the pathogenesis of airway inflammation and obstruction has been recently recognized as a new target for therapeutic intervention (reviewed in Reference 32). They have been shown to increase in the respiratory secretion of children infected with RSV (33,47) and are associated with RSV-induced wheezing (34). In a mouse model of RSV infection, increased levels of cys-LTs correlate with increased airway responsiveness (35), and either inhibition of LT production (35) or treatment with LT receptor antagonist (36) inhibits AHR.…”

Section: Discussionmentioning

confidence: 99%

“…They have been shown to increase in the respiratory secretion of children infected with RSV (33) and are associated with RSV-induced wheezing (34). We and others have shown that inhibition of LT synthesis (35) or treatment with LT receptor antagonist (36) inhibits lung inflammation and AHR in a mouse model of RSV infection.…”

Section: Effect Of Bha On Rsv-induced Lt Productionmentioning

confidence: 99%

See 1 more Smart Citation

Antioxidant Treatment Ameliorates Respiratory Syncytial Virus–induced Disease and Lung Inflammation

Castro

Guerrero-Plata

Suarez-Real

et al. 2006

Am J Respir Crit Care Med

146

154

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Section: Discussionmentioning

confidence: 99%

Section: Effect Of Bha On Rsv-induced Lt Productionmentioning

confidence: 99%

Antioxidant Treatment Ameliorates Respiratory Syncytial Virus–induced Disease and Lung Inflammation

Castro

Guerrero-Plata

Suarez-Real

et al. 2006

Am J Respir Crit Care Med

146

154

View full text Add to dashboard Cite

“…Clinical data support the possible involvement of eosinophils in virus-induced exacerbations and increased airway hyperresponsiveness in asthmatic patients: experimental infections with RV16 led to increases in eosinophils and ECP levels in the airways and to airway hyperresponsiveness in atopic asthmatics [15][16][17]. In infants with respiratory syncytial virus (RSV) bronchiolitis, ECP and LTC 4 levels in upper airway secretions are significantly associated [29]. In a guinea pig model of asthma, both airway responsiveness and eosinophil accumulation in the airways increased after a respiratory infection with parainfluenza-3 virus [30].…”

Section: Ifn-b and Eosinophil-endothelial Cell Adhesionmentioning

confidence: 98%

Interferon-β augments eosinophil adhesion-inducing activity of endothelial cells

Kobayashi

Takaku²,

Yokote³

et al. 2008

Eur Respir J

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Viral infections induce exacerbations of asthma. One of the earliest host responses to viral infections is the production of innate cytokines including type I interferons (IFNs), such as IFN-b, which may act to modify airway inflammation. The objective of the present study was to investigate whether IFN-b modifies the eosinophil adhesion-inducing activity of endothelial cells.Human umbilical vein endothelial cells (HUVECs) were stimulated with IFN-b for 24 h in the presence or absence of tumour necrosis factor (TNF)-a. Eosinophils were isolated from the peripheral blood of healthy volunteers. The ability of the IFN-b-stimulated HUVEC monolayers to induce eosinophil adhesion was assessed according to the eosinophil peroxidase assay.Eosinophil adhesion to HUVECs was significantly augmented by IFN-b in the presence of TNF-a but not in its absence. The augmented adhesion was inhibited by anti-a 4 integrin monoclonal antibody (mAb) or anti-b 2 integrin mAb. IFN-b significantly enhanced the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 on HUVECs in the presence of TNF-a.Interferon-b can augment the adhesiveness of endothelial cells to eosinophils, mainly through the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. This action of interferon-b may contribute to the intensification of airway inflammation in asthma that is associated with exacerbations induced by viral infections.

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“…Leukotriene C 4 within upper airway secretions in infants with RSV bronchiolitis is likely to originate from the eosinophils [16]. It has been suggested that eotaxin-3 is specifically involved in late-phase asthmatic response, facts which may not fully explain the exacerbation of asthma during or after viral airway infection.…”

mentioning

confidence: 93%

dsRNA enhances eotaxin-3 production through interleukin-4 receptor upregulation in airway epithelial cells

Tsuji

Yamamoto²,

Wei-lin³

et al. 2005

Eur Respir J

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The exacerbation of asthma during viral infections is mainly explained by neutrophils infiltrating into the airways. However, enhanced functions of eosinophils are also observed. The aim of this study was to reveal the mechanism of how eosinophils are activated during and after viral infection of the airways, using a model of viral infection.A synthetic double-stranded RNA, poly inosinic-cytidyric acid (poly(IC)), was transfected to a human airway epithelial cell line (BEAS-2B) and the primary bronchial epithelial cells, to mimic a viral infection. The production of chemokines from the cells was investigated.The transfection of poly(IC), alone, marginally affected the eotaxin-3 production of the cells. However, the transfection of poly(IC) prior to interleukin (IL)-4 stimulation enhanced eotaxin-3 production. Poly(IC) transfection increased mRNA and protein expressions of IL-4 receptor (R)a and IL-2Rc, components of the IL-4R. In BEAS-2B cells, IL-4-mediated phosphorylation of signal transducer and activator of transcription six was enhanced in poly(IC) transfected cells. This was reversed by the addition of anti-IL-4Ra antibody, suggesting the role of an increased number of IL-4 receptors in enhanced IL-4-induced eotaxin-3 production. Poly(IC)-induced upregulation of IL4Ra was inhibited by treatment with cycloheximide or dexamethasone.In conclusion, these results suggest that viral airway infection may enhance interleukin-4-induced eotaxin-3 production through upregulation of the interleukin-4 receptor in airway epithelial cells.

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Eosinophil activation and cysteinyl leukotriene production in infants with respiratory syncytial virus bronchiolitis

Cited by 60 publications

References 34 publications

Antioxidant Treatment Ameliorates Respiratory Syncytial Virus–induced Disease and Lung Inflammation

Antioxidant Treatment Ameliorates Respiratory Syncytial Virus–induced Disease and Lung Inflammation

Interferon-β augments eosinophil adhesion-inducing activity of endothelial cells

dsRNA enhances eotaxin-3 production through interleukin-4 receptor upregulation in airway epithelial cells

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