Granulocyte-macrophage Colony Stimulating Factor (GM-CSF) and Interleukin 8 (IL-8) Production by Human Bronchial Epithelial Cells (HBEC) in Asthmatics and Controls. Lack of In Vitro Effect of Salbutamol Compared to Sodium Nedocromil

Gormand, F.; Cheria-Sammari, S.; Aloui, R.; Guibert, Benoît; Malicier, D.; Perrin‐Fayolle, M; Lagarde, Michel; Pachéco, Yves

doi:10.1006/pulp.1995.1013

Cited by 14 publications

(10 citation statements)

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“…It could be assumed that IL‐8, which is increased in BAL fluid following exposure, is responsible for the neutrophil influx into the airways. The pro‐inflammatory cytokine TNF‐α is of importance for the release of IL‐8 as shown in human bronchial epithelial cells in vitro [39]. In the present study, however, inhibition of TNF‐α by SCG did not influence BAL fluid levels of IL‐8 which was unaffected by treatment with SCG.…”

Section: Discussioncontrasting

confidence: 63%

Sodium cromoglycate attenuates pulmonary inflammation without influencing bronchial responsiveness in healthy subjects exposed to organic dust

Larsson¹,

Larsson²,

Sandström

et al. 2001

Clin Experimental Allergy

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Section: Discussioncontrasting

confidence: 63%

Sodium cromoglycate attenuates pulmonary inflammation without influencing bronchial responsiveness in healthy subjects exposed to organic dust

Larsson¹,

Larsson²,

Sandström

et al. 2001

Clin Experimental Allergy

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“…It has been reported that a β 2 ‐agonist, sulbutamol, does not inhibit release of IL‐8 from BECs in response to 2 ng·mL ‐1 TNF‐α[6]. Inhibition of ECA release by procaterol and theophylline occurred at a concentration of 100 U·mL ‐1 TNF‐α and 50 pg·mL ‐1 IL‐1β in the present study.…”

Section: Discussioncontrasting

confidence: 43%

“…Bronchial epithelial cells (BEC) release chemotactic activity for inflammatory cells, including eosinophils [4, 5]. Interleukin (IL)‐8 [6, 7], granulocyte colony‐stimulating factor [7], granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) [6], transforming growth factor‐β (TGF‐β) [8], regulated on activation, normal T‐cell expressed and secreted (RANTES) [9], monocyte chemotactic protein (MCP)‐1 [10], MCP‐4 [11], eotaxin [12], and eicosanoids [4, 5] are thought to be involved in the release of chemotactic factors in response to a variety of stimuli. Thus, BECs actively participate in the airway pathophysiology of asthma, including the bronchial inflammation.…”

mentioning

confidence: 99%

Procaterol inhibits IL-1β- and TNF-α-mediated epithelial cell eosinophil chemotactic activity

et al. 1999

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Theophylline inhibits eosinophilic infiltration into the bronchial wall. It is unknown whether this is mediated by a cyclic adenosine monophosphate (c-AMP) -dependent reduction in eosinophil chemotactic activity (ECA) from bronchial epithelial cells (BEC). Therefore the effect of a b 2 -agonist, procaterol and theophylline on the release of ECA from a BEC line, BEAS-2B was evaluated in response to interleukin (IL)-1b and tumour necrosis factor-a (TNF-a).ECA was assessed using a blind-well chemotactic chamber, and the release and gene expression of cytokines were evaluated by means of enzyme-linked immunosorbent assay and reverse transcriptase polymerase chain reaction.IL-1b and TNF-a stimulated the release of ECA from BEAS-2B cells in a dose-and time-dependent manner. Procaterol and theophylline directly inhibited eosinophil migration to IL-1b and TNF-a-conditioned medium. The pretreatment of BEAS-2B cells with the same concentrations of procaterol inhibited the release of ECA in a dosedependent fashion. Anti-IL-8, anti-regulated on activation, normal T-cell expressed and secreted (RANTES), and anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) inhibited ECA. Procaterol inhibited the release of RANTES, GM-CSF and IL-8 in a dose-dependent fashion. The effect of theophylline was less potent. Procaterol augmented cAMP levels in BEAS-2B cells in a time-and dose-dependent manner. The expression of IL-8, RANTES, and GM-CSF messenger ribonucleic acid was not inhibited by procaterol and theophylline.These data indicate that procaterol and theophylline may directly inhibit eosinophil migration and that procaterol may further inhibit the release of eosinophil chemotactic activity from BEAS-2B cells via a cyclic adenosine monophosphate-dependent mechanism. This warrants further studies on the involvement of bronchial epithelial cells in the anti-inflammatory effects of procaterol and theophylline in patients with asthma. Eur Respir J 1999; 14: 767±775.

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“…Bronchial cells produced cytokines such as GM‐CSF, IL‐6 in vivo and in vitro . TNF‐α or IL‐1β increased the basal production of these cytokines [19, 20]. The next experiment asked whether CD40 L–CD40 interactions affected IL‐6 and GM‐CSF secretions by bronchial cell lines.…”

Section: Resultsmentioning

confidence: 99%

“…We analysed whether CD40 activation could induce cytokine release by bronchial epithelial cell lines. IL‐6 and GM‐CSF are both secreted at a low level by human bronchial cells under basal conditions [19, 20], as was the case in the two cell lines tested. While TNF‐α clearly stimulated the secretion of the two cytokines, CD40 activation did not have such an effect.…”

Section: Discussionmentioning

confidence: 99%

CD40 Expression by Human Bronchial Epithelial Cells

Gormand

Brière²,

Peyrol

et al. 1999

Scand J Immunol

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CD40 is a 50-kDa protein expressed on B cells, dendritic cells, monocytes and epithelial cells, but the distribution of CD40 expression in humans is not completely known. It binds to a ligand (CD40L) which is expressed essentially on activated T cells. The interaction between CD40 and CD40L plays important roles in immune responses. CD40 expression was investigated on bronchial tissues and human bronchial cell lines using immunohistochemistry, immunofluorescence staining and analysis with a cytometer, respectively. Constitutive CD40 expression, but not that of CD40L, was slightly detectable on normal human bronchial epithelial cells (HBEC) in situ and on an adult lung adenocarcinoma (SKLU1) cell line, while another cell line, a bronchial transformed SV40 cell line (WI26VA4), was negative for CD40. Among the various cytokines tested, only interferon (IFN)-gamma was found to induce CD40 expression on WI26VA4. Tumour necrosis factor (TNF)-alpha was the best cytokine able to up-regulate CD40 in SKLU1 cells. A combination of IFN-gamma and TNF-alpha was slightly more effective than the cytokine alone at up-regulating CD40 expression on both cell lines. We further investigated the functional consequences of CD40 ligation on both cell lines. These bronchial cells expressed CD40, HLADR and CD54 under basal conditions or when stimulated by cytokines. Stimulation through CD40 did not affect cell-surface-antigen expression on either cell line. The production of cytokines such as interleukin (IL)-6 and granulocyte macrophage-colony stimulating factor (GM-CSF) by HBEC has been described. SKLU1 and WI26VA4 cells released IL-6 and GM-CSF spontaneously. Whatever the case, CD40 engagement did not modulate spontaneous or TNF-alpha-induced production of these two cytokines. These data indicate for the first time that normal HBEC express CD40 in situ. Further investigations are required in order to determine the role of CD40 on normal HBEC.

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Granulocyte-macrophage Colony Stimulating Factor (GM-CSF) and Interleukin 8 (IL-8) Production by Human Bronchial Epithelial Cells (HBEC) in Asthmatics and Controls. Lack of In Vitro Effect of Salbutamol Compared to Sodium Nedocromil

Cited by 14 publications

References 0 publications

Sodium cromoglycate attenuates pulmonary inflammation without influencing bronchial responsiveness in healthy subjects exposed to organic dust

Sodium cromoglycate attenuates pulmonary inflammation without influencing bronchial responsiveness in healthy subjects exposed to organic dust

Procaterol inhibits IL-1β- and TNF-α-mediated epithelial cell eosinophil chemotactic activity

CD40 Expression by Human Bronchial Epithelial Cells

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