β2long-acting and anticholinergic drugs synergistically control TGFβ1-mediated neutrophilic inflammation in COPD: an “in vitro” model.

    Risultato della ricerca: Other contribution

    Abstract

    TGFβ1 is involved in airway inflammation in COPD and in the regulation of muscarinic receptors (mAChRs) expression. We quantified TGFβ1 and Acetylcholine (ACh) concentrations in induced sputum supernatants (ISs) from 10 Healthy Controls (HC), 14 Healthy Smokers (HS) and 16 COPDs. We tested: 1) ISs from HC, HS and COPD on neutrophil adhesion to human bronchial epithelial cells (16HBE) in the presence or absence of an anti-TGFβ1ab or Olodaterol (β2-adrenoceptor agonist) and Tiotropium (Spiriva®) alone or in combination; 2) ISs from COPD on mAChRs expression in 16HBE in the presence or absence of anti-TGFβ1-antibody and Olodaterol; 3) hrTGFβ1on neutrophil adhesion and mChRs and ChAT expression in 16HBE. We showed that: 1) TGFβ1 and ACh concentrations are increased in ISs from COPD in comparison with HC and HS; 2) ISs from COPD caused higher levels of neutrophil adhesion to 16HBE than ISs from HC and HS and this was significantly reduced by TGFβ1 depletion and by the addition of Olodaterol or Tiotropium alone with a synergistic effect when the drugs were used in combination; 3) mAChR2, mAChR3 and ChAT expression was increased in 16HBE stimulated with ISSs from COPD and are reduced by TGFβ1 depletion while not by Olodaterol; 4) in vitro experiments we confirmed that hrTGFβ1 increases mAChR2, mAChR3 and ChAT expression. These findings suggest that TGFβ1 and mAChRs promote neutrophil adhesion to bronchial epithelial cells during airway inflammation in COPD. Olodaterol and Tiotropium used in combination might synergistically control this proinflammatory event in COPD.
    Lingua originaleEnglish
    Stato di pubblicazionePublished - 2011

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    Drug and Narcotic Control
    Cholinergic Antagonists
    Chronic Obstructive Pulmonary Disease
    Inflammation
    Sputum
    Neutrophils
    Acetylcholine
    Epithelial Cells
    In Vitro Techniques
    Muscarinic Receptors
    Adrenergic Receptors
    Anti-Idiotypic Antibodies

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    title = "β2long-acting and anticholinergic drugs synergistically control TGFβ1-mediated neutrophilic inflammation in COPD: an “in vitro” model.",
    abstract = "TGFβ1 is involved in airway inflammation in COPD and in the regulation of muscarinic receptors (mAChRs) expression. We quantified TGFβ1 and Acetylcholine (ACh) concentrations in induced sputum supernatants (ISs) from 10 Healthy Controls (HC), 14 Healthy Smokers (HS) and 16 COPDs. We tested: 1) ISs from HC, HS and COPD on neutrophil adhesion to human bronchial epithelial cells (16HBE) in the presence or absence of an anti-TGFβ1ab or Olodaterol (β2-adrenoceptor agonist) and Tiotropium (Spiriva{\circledR}) alone or in combination; 2) ISs from COPD on mAChRs expression in 16HBE in the presence or absence of anti-TGFβ1-antibody and Olodaterol; 3) hrTGFβ1on neutrophil adhesion and mChRs and ChAT expression in 16HBE. We showed that: 1) TGFβ1 and ACh concentrations are increased in ISs from COPD in comparison with HC and HS; 2) ISs from COPD caused higher levels of neutrophil adhesion to 16HBE than ISs from HC and HS and this was significantly reduced by TGFβ1 depletion and by the addition of Olodaterol or Tiotropium alone with a synergistic effect when the drugs were used in combination; 3) mAChR2, mAChR3 and ChAT expression was increased in 16HBE stimulated with ISSs from COPD and are reduced by TGFβ1 depletion while not by Olodaterol; 4) in vitro experiments we confirmed that hrTGFβ1 increases mAChR2, mAChR3 and ChAT expression. These findings suggest that TGFβ1 and mAChRs promote neutrophil adhesion to bronchial epithelial cells during airway inflammation in COPD. Olodaterol and Tiotropium used in combination might synergistically control this proinflammatory event in COPD.",
    keywords = "COPD - management, Cell biology, Epithelial cell",
    author = "Albano, {Giusy Daniela}",
    year = "2011",
    language = "English",
    type = "Other",

    }

    TY - GEN

    T1 - β2long-acting and anticholinergic drugs synergistically control TGFβ1-mediated neutrophilic inflammation in COPD: an “in vitro” model.

    AU - Albano, Giusy Daniela

    PY - 2011

    Y1 - 2011

    N2 - TGFβ1 is involved in airway inflammation in COPD and in the regulation of muscarinic receptors (mAChRs) expression. We quantified TGFβ1 and Acetylcholine (ACh) concentrations in induced sputum supernatants (ISs) from 10 Healthy Controls (HC), 14 Healthy Smokers (HS) and 16 COPDs. We tested: 1) ISs from HC, HS and COPD on neutrophil adhesion to human bronchial epithelial cells (16HBE) in the presence or absence of an anti-TGFβ1ab or Olodaterol (β2-adrenoceptor agonist) and Tiotropium (Spiriva®) alone or in combination; 2) ISs from COPD on mAChRs expression in 16HBE in the presence or absence of anti-TGFβ1-antibody and Olodaterol; 3) hrTGFβ1on neutrophil adhesion and mChRs and ChAT expression in 16HBE. We showed that: 1) TGFβ1 and ACh concentrations are increased in ISs from COPD in comparison with HC and HS; 2) ISs from COPD caused higher levels of neutrophil adhesion to 16HBE than ISs from HC and HS and this was significantly reduced by TGFβ1 depletion and by the addition of Olodaterol or Tiotropium alone with a synergistic effect when the drugs were used in combination; 3) mAChR2, mAChR3 and ChAT expression was increased in 16HBE stimulated with ISSs from COPD and are reduced by TGFβ1 depletion while not by Olodaterol; 4) in vitro experiments we confirmed that hrTGFβ1 increases mAChR2, mAChR3 and ChAT expression. These findings suggest that TGFβ1 and mAChRs promote neutrophil adhesion to bronchial epithelial cells during airway inflammation in COPD. Olodaterol and Tiotropium used in combination might synergistically control this proinflammatory event in COPD.

    AB - TGFβ1 is involved in airway inflammation in COPD and in the regulation of muscarinic receptors (mAChRs) expression. We quantified TGFβ1 and Acetylcholine (ACh) concentrations in induced sputum supernatants (ISs) from 10 Healthy Controls (HC), 14 Healthy Smokers (HS) and 16 COPDs. We tested: 1) ISs from HC, HS and COPD on neutrophil adhesion to human bronchial epithelial cells (16HBE) in the presence or absence of an anti-TGFβ1ab or Olodaterol (β2-adrenoceptor agonist) and Tiotropium (Spiriva®) alone or in combination; 2) ISs from COPD on mAChRs expression in 16HBE in the presence or absence of anti-TGFβ1-antibody and Olodaterol; 3) hrTGFβ1on neutrophil adhesion and mChRs and ChAT expression in 16HBE. We showed that: 1) TGFβ1 and ACh concentrations are increased in ISs from COPD in comparison with HC and HS; 2) ISs from COPD caused higher levels of neutrophil adhesion to 16HBE than ISs from HC and HS and this was significantly reduced by TGFβ1 depletion and by the addition of Olodaterol or Tiotropium alone with a synergistic effect when the drugs were used in combination; 3) mAChR2, mAChR3 and ChAT expression was increased in 16HBE stimulated with ISSs from COPD and are reduced by TGFβ1 depletion while not by Olodaterol; 4) in vitro experiments we confirmed that hrTGFβ1 increases mAChR2, mAChR3 and ChAT expression. These findings suggest that TGFβ1 and mAChRs promote neutrophil adhesion to bronchial epithelial cells during airway inflammation in COPD. Olodaterol and Tiotropium used in combination might synergistically control this proinflammatory event in COPD.

    KW - COPD - management

    KW - Cell biology

    KW - Epithelial cell

    UR - http://hdl.handle.net/10447/58333

    M3 - Other contribution

    ER -