Neutrophil adherence to lung epithelial cells induce interleukin-8 release.

C. D. Huang, K. H. Huang, H. C. Lin, C. H. Wang, H. P. Kuo

Research output: Contribution to journalArticle

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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.

Original languageEnglish
Pages (from-to)392-399
Number of pages8
JournalChanggeng yi xue za zhi / Changgeng ji nian yi yuan = Chang Gung medical journal / Chang Gung Memorial Hospital
Volume22
Issue number3
Publication statusPublished - Jan 1 1999
Externally publishedYes

Fingerprint

Interleukin-8
Neutrophils
Epithelial Cells
Lung
Interleukin-1beta
Interferon-gamma
Tumor Necrosis Factor-alpha
Cultured Cells
Blocking Antibodies
Neutrophil Infiltration
Intercellular Adhesion Molecule-1
Respiratory System
Down-Regulation
Epithelium
Cytokines
Inflammation
Membranes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Neutrophil adherence to lung epithelial cells induce interleukin-8 release. / Huang, C. D.; Huang, K. H.; Lin, H. C.; Wang, C. H.; Kuo, H. P.

In: Changgeng yi xue za zhi / Changgeng ji nian yi yuan = Chang Gung medical journal / Chang Gung Memorial Hospital, Vol. 22, No. 3, 01.01.1999, p. 392-399.

Research output: Contribution to journalArticle

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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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N2 - 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.

AB - 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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