Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells (Articolo in rivista)

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Label
  • Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells (Articolo in rivista) (literal)
Anno
  • 2008-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1111/j.1365-2567.2007.02788.x (literal)
Alternative label
  • Elisabetta Pace1; Maria Ferraro1,2; Liboria Siena1; Mario Melis1;Angela M. Montalbano1; Malcolm Johnson3; Maria R. Bonsignore4; Giovanni Bonsignore1,* and Mark Gjomarkaj1 (2008)
    Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells
    in Immunology (Oxf., Print)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Elisabetta Pace1; Maria Ferraro1,2; Liboria Siena1; Mario Melis1;Angela M. Montalbano1; Malcolm Johnson3; Maria R. Bonsignore4; Giovanni Bonsignore1,* and Mark Gjomarkaj1 (literal)
Pagina inizio
  • 401 (literal)
Pagina fine
  • 411 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 124 (literal)
Rivista
Note
  • PubMe (literal)
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1Istituto di Biomedicina e Immunologia Molecolare, Consiglio Nazionale delle Ricerche, Palermo, Italy, 2Dipartimento di Anestesiologia, Rianimazione e delle Emergenze, Universita` degli Studi di Palermo, Palermo, Italy, 3GlaxoSmithKline Research and Development Ltd., Greenford, Middlesex, UK, and 4Dipartimento di medicina, pneumologia, fisiologia e nutrizione umana, Universita` degli Studi di Palermo, Palermo, Italy (literal)
Titolo
  • Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells (literal)
Abstract
  • Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke. The main goal of this study was to explore the effects of cigarette smoke extracts (CSE) on Tolllike receptor (TLR) expression and activation in a human bronchial epithelial cell line (16-HBE). The CSE increased the expression of TLR4 and the lipopolysaccharide (LPS) binding, the nuclear factor-jB (NF-jB) activation, the release of interleukin-8 (IL-8) and the chemotactic activity toward neutrophils. It did not induce TLR2 expression or extracellular signal-regulated signal kinase 1/2 (ERK1/2) activation. The LPS increased the expression of TLR4 and induced both NF-jB and ERK1/2 activation. The combined exposure of 16-HBE to CSE and LPS was associated with ERK activation rather than NF-jB activation and with a further increase of IL-8 release and of chemotactic activity toward neutrophils. Furthermore, CSE decreased the constitutive interferon-inducible protein-10 (IP-10) release and counteracted the effect of LPS in inducing both the IP-10 release and the chemotactic activity toward lymphocytes. In conclusion, cigarette smoke, by altering the expression and the activation of TLR4 via the preferential release of IL-8, may contribute to the accumulation of neutrophils within the airways of smokers. (literal)
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