Inhibition of pyocyanin-potentiated IL-8 release by steroids in bronchial epithelial cells

Pan, Nin Y.; Hui, Wing Sze; Tipoe, George L.; Taylor, Graham W.; Leung, R; Lam, Wah Kit; Tsang, K. T.; Mak, Judith C.W.

doi:10.1016/j.rmed.2005.12.003

Cited by 18 publications

(17 citation statements)

References 29 publications

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“…Introduction of salmeterol into the airways of asthmatics has been found to reduce IL-8 and myeloperoxidase levels in bronchoalveolar lavage fluid; in the same study, high-dose inhaled corticosteroid treatment increased rather than decreased airway neutrophils [23]. However, in vitro studies have suggested that there are dose-dependent effects of fluticasone on the inhibition of IL-8 and other mediators released from various types of cells, including airway epithelial cells [24], smooth muscle cells [25] and fibroblasts [26]. A synergistic effect of SFP on the inhibition of mediator release has also been demonstrated [27][28][29][30].…”

Section: Discussionmentioning

confidence: 87%

Anti-inflammatory effects of salmeterol/fluticasone, tiotropium/fluticasone or tiotropium in COPD

Dw¹,

Cw²,

Kc³

et al. 2009

European Respiratory Journal

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The anti-inflammatory effects of salmeterol/fluticasone (SFP), tiotropium/fluticasone (Tio+FP) and tiotropium (Tio) alone were investigated on the inflammatory cells and mediators in sputum induced from chronic obstructive pulmonary disease patients.Subjects were either newly diagnosed or had not taken any medication for 3 months prior to the study. Subjects (n599) were randomised (not double blinded) and received either SFP (100/ 1,000 mg daily), Tio+FP (18/1,000 mg daily) or Tio (18 mg daily) for 12 weeks. Induced sputum and serum C-reactive protein (CRP) were analysed prior to and at the end of treatment.The results showed that treatment with SFP caused a significant reduction in interleukin (IL)-8 and matrix metalloprotease (MMP)-9 in induced sputum, compared with treatment with Tio alone. There were no treatment differences between the SFP and Tio+FP groups in decreasing IL-8 and MMP-9 levels. The reduction in IL-8 showed significant association with the reduction in MMP-9. All treatment groups failed to significantly reduce the numbers of total cells, neutrophils, macrophages and eosinophils in induced sputum; in addition, there were no treatment differences in terms of improvement of forced expiratory volume in one second, forced vital capacity, CRP or quality of life between the three groups.The anti-inflammatory effects of salmeterol/fluticasone probably contribute to the clinical benefits seen in chronic obstructive pulmonary disease patients.

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Section: Discussionmentioning

confidence: 87%

Anti-inflammatory effects of salmeterol/fluticasone, tiotropium/fluticasone or tiotropium in COPD

Dw¹,

Cw²,

Kc³

et al. 2009

European Respiratory Journal

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“…PCN also acts in synergy with IL-1α, IL-1β and TNF-α to induce IL-8 expression [5,6,8]. After PCN was injected into animals and the respiratory tracts, bronchial lavage fluid and neutrophil (PMN) levels were increased significantly [41].…”

Section: Discussionmentioning

confidence: 99%

Pseudomonas pyocyanin stimulates IL-8 expression through MAPK and NF-κB pathways in differentiated U937 cells

et al. 2014

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BackgroundPyocyanin (PCN), an extracellular product of Pseudomonas aeruginosa and a blue redox active secondary metabolite, plays an important role in invasive pulmonary infection. However, the detailed inflammatory response triggered by PCN infection in inflammatory cells (particularly macrophages), if present, remains to be clarified. To investigate the effects of PCN on macrophages, the ability of PCN to induce inflammation reaction and the signaling pathway for IL-8 release in PCN-induced differentiated U937 cells were examined.ResultsIt was found that PCN increased IL-8 release and mRNA expression in Phorbol 12-myristate 13-acetate (PMA) differentiated U937 cells in both a concentration- and time-dependent manner by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). P38 and ERK MAPKs were activated after 10 min of induction with PCN and their levels returned to baselines after 30 min by Western blotting. It was also found that within 10 min of PCN incubation, the level of p-I-κBα in the cytosol was increased, which returned to baseline level after 60 min. Meanwhile, the level of p-p65 was increased in the nuclear extract and cytosol, and maintained high in total cell lysates. The results were further confirmed by the observation that p38, ERK1/2 and NF-κB inhibitors inhibited PCN-induced NF-κB activation and attenuated PCN-induced IL-8 expression in U937 cells as a function of their concentrations. Moreover, it was shown that PCN induced oxidative stress in U937 cells and N-acetyl cysteine, an antioxidant, was able to inhibit PCN-induced IL-8 protein expression.ConclusionsIt is concluded that PCN induces IL-8 secretion and mRNA expression in PMA-differentiated U937 cells in a concentration- and time- dependent manner. Furthermore, p38 and ERK MAPKs and NF-κΒ signaling pathways may be involved in the expression of IL-8 in PCN-incubated PMA-differentiated U937 cells.

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“…Furthermore, Pan et al. () reported that treatment with budesonide (10 −8 mol/L) reduces the release of IL‐8 by 50% in the supernatants of human bronchial epithelial cells (BEAS‐2B) in response to the stimulation with IL‐1β plus pyocyanin, a toxic factor from the bacteria Pseudomonas aeruginosa . In the present study, tulobuterol reduced the release of IL‐8 in supernatants to baseline levels.…”

Section: Discussionmentioning

confidence: 99%

Tulobuterol inhibits rhinovirus infection in primary cultures of human tracheal epithelial cells

et al. 2013

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A transdermal patch preparation of the β2 agonist tulobuterol has been designed to yield sustained β2 agonistic effects and has been used as a long-acting β2 agonist (LABA) in Japan. LABAs reduce the frequency of exacerbations of chronic obstructive pulmonary disease and bronchial asthma. However, inhibitory effects of LABAs on the replication of rhinovirus (RV), the major cause of exacerbations, have not been demonstrated. To examine the effects of tulobuterol on RV replication and on the production of the replication-induced pro-inflammatory cytokines, human tracheal epithelial cells were infected with a major group RV, type 14 rhinovirus (RV14). Tulobuterol reduced the RV14 titers and RNA levels; the concentrations of cytokines, including interleukin (IL)-1β, IL-6, and IL-8, in the supernatants; and susceptibility to RV14 infection. Tulobuterol reduced the expression of intercellular adhesion molecule-1 (ICAM-1), the receptor for RV14, and the number of acidic endosomes in the cells in which RV14 RNA enters the cytoplasm. Tulobuterol inhibited the activation of nuclear factor kappa B (NF-κB) proteins in nuclear extracts. A selective β2-adrenergic receptor antagonist, ICI 118551 [erythro-dl-1-(7-methylindan-4-yloxy)-3-isopropylaminobutan-2-ol], reversed the inhibitory effects of tulobuterol on the RV14 titers and RNA levels, the susceptibility to RV14 infection, cytokine production, and ICAM-1 expression. Tulobuterol may inhibit RV replication by reducing ICAM-1 expression and acidic endosomes and modulate airway inflammation during RV replication.

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Inhibition of pyocyanin-potentiated IL-8 release by steroids in bronchial epithelial cells

Cited by 18 publications

References 29 publications

Anti-inflammatory effects of salmeterol/fluticasone, tiotropium/fluticasone or tiotropium in COPD

Anti-inflammatory effects of salmeterol/fluticasone, tiotropium/fluticasone or tiotropium in COPD

Pseudomonas pyocyanin stimulates IL-8 expression through MAPK and NF-κB pathways in differentiated U937 cells

Tulobuterol inhibits rhinovirus infection in primary cultures of human tracheal epithelial cells

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