RANTES, Macrophage‐Inhibitory Protein 1𝛂, and the Eosinophil Product Major Basic Protein Are Released into Upper Respiratory Secretions during Virus‐Induced Asthma Exacerbations in Children

Teran, Luis M.; Seminario, Maria Cristina; Shute, Janis K.; Papi, Alberto; Compton, Steven J.; Low, J L; Gleich, Gerald J.; Johnston, Sebastian L.

doi:10.1086/314618

Cited by 81 publications

(65 citation statements)

References 16 publications

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“…Even in low concentrations, BAL RANTES incites eosinophil attraction and has been shown to correlate with the proportion of BAL eosinophils (46). Our data demonstrate a reduction in both TGF-b 1 and RANTES in BAL fluid in the weeks after BT applied to a single lobe, which in turn correlated with a decrease in BAL eosinophil proportion throughout the time period of BT treatment.…”

Section: C/fposupporting

confidence: 54%

Airway Inflammation after Bronchial Thermoplasty for Severe Asthma

et al. 2015

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Rationale: Bronchial thermoplasty is an alternative treatment for patients with severe, uncontrolled asthma in which the airway smooth muscle is eliminated using radioablation. Although this emerging therapy shows promising outcomes, little is known about its effects on airway inflammation.Objectives: We examined the presence of bronchoalveolar lavage cytokines and expression of smooth muscle actin in patients with severe asthma before and in the weeks after bronchial thermoplasty.Methods: Endobronchial biopsies and bronchoalveolar lavage samples from 11 patients with severe asthma were collected from the right lower lobe before and 3 and 6 weeks after initial bronchial thermoplasty. Samples were analyzed for cell proportions and cytokine concentrations in bronchoalveolar lavage and for the presence of a-SMA in endobronchial biopsies.Measurements and Main Results: a-SMA expression was decreased in endobronchial biopsies of 7 of 11 subjects by Week 6. In bronchoalveolar lavage fluid, both transforming growth factor-b 1 and regulated upon activation, normal T-cell expressed and secreted (RANTES)/CCL5 were substantially decreased 3 and 6 weeks post bronchial thermoplasty in all patients. The cytokine tumor-necrosisfactor-related apoptosis-inducing ligand (TRAIL), which induces apoptosis in several cell types, was increased in concentration both 3 and 6 weeks post bronchial thermoplasty.Conclusions: Clinical improvement and reduction in a-SMA after bronchial thermoplasty in severe, uncontrolled asthma is associated with substantial changes in key mediators of inflammation. These data confirm the substantial elimination of airway smooth muscle post thermoplasty in the human asthmatic airway and represent the first characterization of significant changes in airway inflammation in the first weeks after thermoplasty.

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Section: C/fposupporting

confidence: 54%

Airway Inflammation after Bronchial Thermoplasty for Severe Asthma

et al. 2015

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“…Viral infection of bronchial epithelial cells is known to induce RANTES secretion and RANTES is implicated in viral diseases, inducing airway inflammation caused by several viral infections in human and animal models [12,13]. However, the mechanisms of inducible RANTES gene expression in airway epithelial cells have not yet been fully demonstrated, although RANTES expression may be a major element in the pathogenesis of viral infection [14].…”

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confidence: 99%

Simvastatin suppresses RANTES-mediated neutrophilia in polyinosinic–polycytidylic acid-induced pneumonia

Lee

et al. 2012

Eur Respir J

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Recently, statins have been shown to have anti-inflammatory effects on lung inflammatory diseases. However, the mechanisms of action of simvastatin in viral pneumonia have yet to be elucidated, although viral infection remains a considerable health threat. In this study, we hypothesised that simvastatin inhibits polyinosinic-polycytidylic acid (poly I:C)-induced airway inflammation, such as RANTES (regulated on activation, normal T-cell expressed and secreted) expression and inflammatory cell recruitment.In bronchial cells, the effect of simvastatin on poly I:C-induced RANTES expression and signal transducer and activator of transcription (STAT)3-mediated signal transduction was determined using an ELISA and short hairpin (sh)RNA system. In a poly I:C-induced pneumonia mouse model, immunological changes in the lungs after simvastatin inhalation, such as inflammatory cell recruitment and cytokine/chemokine release, were examined.In poly I:C-stimulated bronchial cells, RANTES secretion was increased by STAT3 activation, and simvastatin suppressed poly I:C-induced STAT3 activation, resulting in inhibition of RANTES expression. In BALB/c mice stimulated with inhaled poly I:C, RANTES expression and neutrophil infiltration into the airway were elevated. However, simvastatin treatment attenuated STAT3 activation, RANTES release and subsequent neutrophilia in the lungs.These findings suggest that simvastatin inhibits airway inflammation, but there are other mechanisms that need to be fully elucidated.

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“…Administration of RANTES in vitro produces transendothelial migration and degranulation of eosinophils (10) and in vivo eosinophilic inflammation in human upper airways (3). Concentration of RANTES is elevated in the bronchoalveolar lavage fluid of asthmatic patients (2,38) and children with RSV bronchiolitis (11,15,35). Administration of a RANTES receptor antagonist or neutralizing RANTES antibodies completely blocks lung eosinophilia and inflammation in experimental models of asthma (14).…”

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confidence: 99%