{"title":"Neutrophil adherence to lung epithelial cells induce interleukin-8 release.","authors":"C D Huang, K H Huang, H C Lin, C H Wang, H P Kuo","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Neutrophil recruitment to the lungs and transmigration through the pulmonary epithelium to reach the respiratory tract are characteristics of airway inflammation. Interleukin-8 (IL-8) plays a critical role in the recruitment of neutrophils to epithelial cells. We investigated the effect of neutrophil adherence to epithelial cells on cytokine secretion.</p><p><strong>Methods: </strong>The production of IL-8 from cultured A549 epithelial cells was assayed and neutrophil adherence assay in the presence or absence of interferon-gamma (IFN-gamma) plus tumor necrosis factor-alpha (TNF-alpha) plus interleukin-1 beta (IL-1 beta) stimulation was studied on cultured A549 epithelial cells. The role of an adhesion molecule in the modulation of neutrophil adherence was examined by pretreatment with intercellular adhesion molecule-1 (ICAM-1) blocking antibody.</p><p><strong>Results: </strong>There was an increase in IL-8 release from epithelial cells that was time-dependent and in the magnitude of neutrophil adherence to the epithelial cells. Stimulation of epithelial cells with IFN-gamma +TNF-alpha +IL-1 beta significantly increased IL-8 release and neutrophil adherence. The spontaneous or IFN-gamma +TNF-alpha +IL-1 beta-induced IL-8 release was significantly augmented after the addition of neutrophils. The inhibition of neutrophil adherence to epithelial cells by ICAM-1 blocking antibody downregulated the augmented release of IL-8 with or without IFN-gamma +TNF-alpha +IL-1 beta stimulation. Placing a membrane filter on cultured epithelial cells to prevent neutrophil adherence significantly decreased IL-8 release from epithelial cells with IFN-gamma +TNF-alpha +IL-1 beta stimulation.</p><p><strong>Conclusion: </strong>Our results indicate that lung epithelial cells not only provide a harboring site for neutrophils to be activated, but also amplify the neutrophil sequestration in the lung by releasing IL-8. Moreover, the release of IL-8 is dependent on the adherence between neutrophils and lung epithelial cells.</p>","PeriodicalId":77066,"journal":{"name":"Changgeng yi xue za zhi","volume":"22 3","pages":"392-9"},"PeriodicalIF":0.0000,"publicationDate":"1999-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Changgeng yi xue za zhi","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Neutrophil recruitment to the lungs and transmigration through the pulmonary epithelium to reach the respiratory tract are characteristics of airway inflammation. Interleukin-8 (IL-8) plays a critical role in the recruitment of neutrophils to epithelial cells. We investigated the effect of neutrophil adherence to epithelial cells on cytokine secretion.
Methods: The production of IL-8 from cultured A549 epithelial cells was assayed and neutrophil adherence assay in the presence or absence of interferon-gamma (IFN-gamma) plus tumor necrosis factor-alpha (TNF-alpha) plus interleukin-1 beta (IL-1 beta) stimulation was studied on cultured A549 epithelial cells. The role of an adhesion molecule in the modulation of neutrophil adherence was examined by pretreatment with intercellular adhesion molecule-1 (ICAM-1) blocking antibody.
Results: There was an increase in IL-8 release from epithelial cells that was time-dependent and in the magnitude of neutrophil adherence to the epithelial cells. Stimulation of epithelial cells with IFN-gamma +TNF-alpha +IL-1 beta significantly increased IL-8 release and neutrophil adherence. The spontaneous or IFN-gamma +TNF-alpha +IL-1 beta-induced IL-8 release was significantly augmented after the addition of neutrophils. The inhibition of neutrophil adherence to epithelial cells by ICAM-1 blocking antibody downregulated the augmented release of IL-8 with or without IFN-gamma +TNF-alpha +IL-1 beta stimulation. Placing a membrane filter on cultured epithelial cells to prevent neutrophil adherence significantly decreased IL-8 release from epithelial cells with IFN-gamma +TNF-alpha +IL-1 beta stimulation.
Conclusion: Our results indicate that lung epithelial cells not only provide a harboring site for neutrophils to be activated, but also amplify the neutrophil sequestration in the lung by releasing IL-8. Moreover, the release of IL-8 is dependent on the adherence between neutrophils and lung epithelial cells.
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