Nebulized hypertonic saline decreases IL-8 in sputum of patients with cystic fibrosis.

Hdl Handle:
http://hdl.handle.net/10147/141079
Title:
Nebulized hypertonic saline decreases IL-8 in sputum of patients with cystic fibrosis.
Authors:
Reeves, Emer P; Williamson, Michael; O'Neill, Shane J; Greally, Peter; McElvaney, Noel G
Affiliation:
Respiratory Research Division, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin 9, Ireland. emerreeves@rcsi.ie
Citation:
Nebulized hypertonic saline decreases IL-8 in sputum of patients with cystic fibrosis. 2011, 183 (11):1517-23 Am. J. Respir. Crit. Care Med.
Journal:
American journal of respiratory and critical care medicine
Issue Date:
1-Jun-2011
URI:
http://hdl.handle.net/10147/141079
DOI:
10.1164/rccm.201101-0072OC
PubMed ID:
21330456
Additional Links:
http://www.ncbi.nlm.nih.gov/pubmed/21330456
Abstract:
Inflammation within the cystic fibrosis (CF) lung is mediated by inflammatory chemokines, such as IL-8. IL-8 is protected from proteolytic degradation in the airways by binding to glycosaminoglycans, while remaining active. Evidence that increased hypertonicity of airway secretions induced by hypertonic saline treatment alters levels of IL-8 is lacking.; To investigate the antiinflammatory effect of hypertonic saline (HTS) treatment within the CF lung by focusing on IL-8.; Degradation of IL-8 in CF lung secretions after treatment with glycosaminoglycan lyases and HTS was analyzed by Western blot analysis and ELISA. The ex vivo chemotactic activity of purified neutrophils in response to CF airway secretions was evaluated post nebulization of HTS (7% saline).; In vivo CF bronchoalveolar lavage fluid (BALF) IL-8 levels were significantly higher than the control group (P < 0.05). Digesting glycosaminoglycans in CF BALF displaced IL-8 from glycosaminoglycan matrices, rendering the chemokine susceptible to proteolytic cleavage. High sodium concentrations also liberate IL-8 in CF BALF in vitro, and in vivo in CF sputum from patients receiving aerosolized HTS, resulting in degradation of IL-8 and decreased neutrophil chemotactic efficiency.; Glycosaminoglycans possess the ability to influence the chemokine profile of the CF lung by binding and stabilizing IL-8, which promotes neutrophil chemotaxis and activation. Nebulized hypertonic saline treatment disrupts the interaction between glycosaminoglycans and IL-8, rendering IL-8 susceptible to proteolytic degradation with subsequent decrease in neutrophil chemotaxis, thereby facilitating resolution of inflammation.
Item Type:
Article
Language:
en
MeSH:
Administration, Inhalation; Adult; Blotting, Western; Bronchoalveolar Lavage Fluid; Cystic Fibrosis; Electrophoresis, Polyacrylamide Gel; Enzyme-Linked Immunosorbent Assay; Glycosaminoglycans; Humans; Inflammation; Interleukin-8; Middle Aged; Nebulizers and Vaporizers; Saline Solution, Hypertonic; Sputum; Young Adult
ISSN:
1535-4970

Full metadata record

DC FieldValue Language
dc.contributor.authorReeves, Emer Pen
dc.contributor.authorWilliamson, Michaelen
dc.contributor.authorO'Neill, Shane Jen
dc.contributor.authorGreally, Peteren
dc.contributor.authorMcElvaney, Noel Gen
dc.date.accessioned2011-08-29T10:31:49Z-
dc.date.available2011-08-29T10:31:49Z-
dc.date.issued2011-06-01-
dc.identifier.citationNebulized hypertonic saline decreases IL-8 in sputum of patients with cystic fibrosis. 2011, 183 (11):1517-23 Am. J. Respir. Crit. Care Med.en
dc.identifier.issn1535-4970-
dc.identifier.pmid21330456-
dc.identifier.doi10.1164/rccm.201101-0072OC-
dc.identifier.urihttp://hdl.handle.net/10147/141079-
dc.description.abstractInflammation within the cystic fibrosis (CF) lung is mediated by inflammatory chemokines, such as IL-8. IL-8 is protected from proteolytic degradation in the airways by binding to glycosaminoglycans, while remaining active. Evidence that increased hypertonicity of airway secretions induced by hypertonic saline treatment alters levels of IL-8 is lacking.-
dc.description.abstractTo investigate the antiinflammatory effect of hypertonic saline (HTS) treatment within the CF lung by focusing on IL-8.-
dc.description.abstractDegradation of IL-8 in CF lung secretions after treatment with glycosaminoglycan lyases and HTS was analyzed by Western blot analysis and ELISA. The ex vivo chemotactic activity of purified neutrophils in response to CF airway secretions was evaluated post nebulization of HTS (7% saline).-
dc.description.abstractIn vivo CF bronchoalveolar lavage fluid (BALF) IL-8 levels were significantly higher than the control group (P < 0.05). Digesting glycosaminoglycans in CF BALF displaced IL-8 from glycosaminoglycan matrices, rendering the chemokine susceptible to proteolytic cleavage. High sodium concentrations also liberate IL-8 in CF BALF in vitro, and in vivo in CF sputum from patients receiving aerosolized HTS, resulting in degradation of IL-8 and decreased neutrophil chemotactic efficiency.-
dc.description.abstractGlycosaminoglycans possess the ability to influence the chemokine profile of the CF lung by binding and stabilizing IL-8, which promotes neutrophil chemotaxis and activation. Nebulized hypertonic saline treatment disrupts the interaction between glycosaminoglycans and IL-8, rendering IL-8 susceptible to proteolytic degradation with subsequent decrease in neutrophil chemotaxis, thereby facilitating resolution of inflammation.-
dc.language.isoenen
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/21330456en
dc.subject.meshAdministration, Inhalation-
dc.subject.meshAdult-
dc.subject.meshBlotting, Western-
dc.subject.meshBronchoalveolar Lavage Fluid-
dc.subject.meshCystic Fibrosis-
dc.subject.meshElectrophoresis, Polyacrylamide Gel-
dc.subject.meshEnzyme-Linked Immunosorbent Assay-
dc.subject.meshGlycosaminoglycans-
dc.subject.meshHumans-
dc.subject.meshInflammation-
dc.subject.meshInterleukin-8-
dc.subject.meshMiddle Aged-
dc.subject.meshNebulizers and Vaporizers-
dc.subject.meshSaline Solution, Hypertonic-
dc.subject.meshSputum-
dc.subject.meshYoung Adult-
dc.titleNebulized hypertonic saline decreases IL-8 in sputum of patients with cystic fibrosis.en
dc.typeArticleen
dc.contributor.departmentRespiratory Research Division, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin 9, Ireland. emerreeves@rcsi.ieen
dc.identifier.journalAmerican journal of respiratory and critical care medicineen
dc.description.provinceLeinster-

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