Isoproterenol suppresses cytokine-induced RANTES secretion in human lung epithelial cells through the inhibition of c-jun N-terminal kinase pathway

Chemokine CC‐ligand 5 production and eosinophil activation into the upper airways of aspirin‐sensitive patients

“…In order to investigate the cellular source of CCL5, we have performed immunohistochemical staining of nasal tissue obtained from patients undergoing nasal surgery. CCL5 can be produced by several cells implicated in the airway inflammatory response in AERD including eosinophils [27], T‐lymphocytes [15], monocytes [28] fibroblasts [29], vascular endothelial cells [30, 31] and airway epithelial cells [32, 33]. However, we have demonstrated that immunoreactivity was predominantly localized to the nasal epithelium, which was found to be increased in ASA‐sensitive as compared with ASA‐tolerant patients.…”

Human Embryonic Stem Cells Differentiated to Lung Lineage-Specific Cells Ameliorate Pulmonary Fibrosis in a Xenograft Transplant Mouse Model

“…Through this canonical Wnt signaling pathway, β-catenin increases in the nucleus and forms a complex with T cell factor (TCF)/lymphoid enhancer factor-1 (LEF-1) transcription factors that are differentiately modulated by Creb-binding protein (CBP) and p300 co-activators. An increase in β-catenin/CBP-mediated transcription by selectively inhibiting β-catenin/p300-mediated transcription maintains stem cell pluripotency, whereas blockade of β-catenin/CBP signaling facilitates β-catenin/p300-mediated transcription and cell differentiation [14]–[16].…”

Can β2‐adrenoceptor agonists, anticholinergic drugs, and theophylline contribute to the control of pulmonary inflammation and emphysema in COPD?

“…A lipopolysaccharide (LPS)-induced tumor necrosis factor a (TNF-a) and granulocyte-macrophage colony-stimulating factor (GM-CSF) release from monocyte-derived macrophages can be significantly inhibited by formoterol or salmeterol [27]. Other studies on airway epithelial cells stimulated Albuterol Reduction in GM-CSF expression and production [169] Isoproterenol Inhibition of the release of RANTES [170] Formoterol Reduction in GM-CSF release [29] Rhinovirus Formoterol Suppression of production of CXCL8 and bFGF [171] TNF-a Formoterol, salmeterol Reduction in IL-8, GM-CSF and VEGF secretion [30] Lung myofibroblasts TNF-a Salmeterol Decrease in IL-6 release and nuclear translocation of NF-kB [172] Mast cells IgE Salbutamol Salmeterol Inhibition of TNF-a release [173] Salmeterol Reduction in histamine release [31] Alveolar macrophages Endotoxin Formoterol, salmeterol Reduction in TNF-a and GM-CSF release [174] Salbutamol Formoterol Reduction in superoxide anion O À 2 release and bacterial killing [22] NTHi by TNF-a also illustrate the anti-inflammatory activity of b 2 -adrenoceptor agonists such as formoterol and salmeterol through a reduction of interleukin 8 (IL-8), GM-CSF, and vascular endothelial growth factor (VEGF) secretion [29,30]. Other studies on airway epithelial cells stimulated Albuterol Reduction in GM-CSF expression and production [169] Isoproterenol Inhibition of the release of RANTES [170] Formoterol Reduction in GM-CSF release [29] Rhinovirus Formoterol Suppression of production of CXCL8 and bFGF [171] TNF-a Formoterol, salmeterol Reduction in IL-8, GM-CSF and VEGF secretion [30] Lung myofibroblasts TNF-a Salmeterol Decrease in IL-6 release and nuclear translocation of NF-kB [172] Mast cells IgE Salbutamol Salmeterol Inhibition of TNF-a release [173] Salmeterol Reduction in histamine release [31] Alveolar macrophages Endotoxin Formoterol, salmeterol Reduction in TNF-a and GM-CSF release [174] Salbutamol Formoterol Reduction in superoxide anion O À 2 release and bacterial killing [22] NTHi by TNF-a also illustrate the anti-inflammatory activity of b 2 -adrenoceptor agonists such as formoterol and salmeterol through a reduction of interleukin 8 (IL-8), GM-CSF, and vascular endothelial growth factor (VEGF) secretion [29,…”