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

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 journal › Article › peer-review

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 language	English
Pages (from-to)	392-399
Number of pages	8
Journal	Changgeng yi xue za zhi / Changgeng ji nian yi yuan = Chang Gung medical journal / Chang Gung Memorial Hospital
Volume	22
Issue number	3
Publication status	Published - Jan 1 1999
Externally published	Yes

ASJC Scopus subject areas

General Medicine

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title = "Neutrophil adherence to lung epithelial cells induce interleukin-8 release.",

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.",

author = "Huang, {C. D.} and Huang, {K. H.} and Lin, {H. C.} and Wang, {C. H.} and Kuo, {H. P.}",

year = "1999",

month = jan,

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language = "English",

volume = "22",

pages = "392--399",

journal = "Changgeng yi xue za zhi / Changgeng ji nian yi yuan = Chang Gung medical journal / Chang Gung Memorial Hospital",

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publisher = "Chang Gung Medical Journal",

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TY - JOUR

T1 - Neutrophil adherence to lung epithelial cells induce interleukin-8 release.

AU - Huang, C. D.

AU - Huang, K. H.

AU - Lin, H. C.

AU - Wang, C. H.

AU - Kuo, H. P.

PY - 1999/1/1

Y1 - 1999/1/1

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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AN - SCOPUS:0033192402

SN - 0255-8270

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JO - Changgeng yi xue za zhi / Changgeng ji nian yi yuan = Chang Gung medical journal / Chang Gung Memorial Hospital

JF - Changgeng yi xue za zhi / Changgeng ji nian yi yuan = Chang Gung medical journal / Chang Gung Memorial Hospital

IS - 3

ER -

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

Abstract

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