Resting and cytokine-stimulated human small airway epithelial cells recognize and engulf apoptotic eosinophils

G M Walsh, D W Sexton, M G Blaylock, C M Convery

Research output: Contribution to journalArticle

75 Citations (Scopus)

Abstract

Eosinophils, which are prominent cells in asthmatic inflammation, undergo apoptosis and are recognized and engulfed by phagocytic macrophages in vitro. We have examined the ability of human small airway epithelial cells (SAEC) to recognize and ingest apoptotic human eosinophils, Cultured SAEC ingested apoptotic eosinophils but not freshly isolated eosinophils or opsonized erythrocytes. The ability of SAEC to ingest apoptotic eosinophils was enhanced by interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor alpha (TNF alpha) in a time- and concentration-dependent fashion. IL-1 alpha was found to be more potent than TNF alpha and each was optimal at 10(-10) mol/L, with a significant (P < .05) effect observed at 1 hour postcytokine incubation that was maximal at 5 hours. IL-1 alpha stimulation not only increased the number of SAEC engulfing apoptotic eosinophils, but also enhanced their capacity for ingestion. The amino sugars glucosamine, n-acetyl glucosamine, and galactosamine significantly inhibited uptake of apoptotic eosinophils by both resting and IL-1 alpha-stimulated SAEC, in contrast to the parent sugars glucose, galactose, mannose, and fucose. Incubation of apoptotic eosinophils with the tetrapeptide RGDS, but not RGES, significantly inhibited their uptake by both resting and IL-1 alpha-stimulated SAEC, as did monoclonal antibody against alpha v beta 3 and CD36. Thus, SAEC recognize apoptotic eosinophils via lectin- and integrin-dependent mechanisms. These data demonstrate a novel function for human bronchial epithelial cells that might represent an important mechanism in the resolution of eosinophil-induced asthmatic inflammation. (C) 1999 by The American Society of Hematology.

Original languageEnglish
Pages (from-to)2827-2835
Number of pages9
JournalBlood
Volume94
Publication statusPublished - 1999

Keywords

  • VITRONECTIN RECEPTOR
  • IN-VITRO
  • MACROPHAGE RECOGNITION
  • MONOCLONAL-ANTIBODIES
  • MEDIATED PHAGOCYTOSIS
  • DENDRITIC CELLS
  • DEATH
  • NEUTROPHILS
  • PHOSPHATIDYLSERINE
  • ASTHMA

Cite this

Resting and cytokine-stimulated human small airway epithelial cells recognize and engulf apoptotic eosinophils. / Walsh, G M ; Sexton, D W ; Blaylock, M G ; Convery, C M .

In: Blood, Vol. 94, 1999, p. 2827-2835.

Research output: Contribution to journalArticle

Walsh, G M ; Sexton, D W ; Blaylock, M G ; Convery, C M . / Resting and cytokine-stimulated human small airway epithelial cells recognize and engulf apoptotic eosinophils. In: Blood. 1999 ; Vol. 94. pp. 2827-2835.
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abstract = "Eosinophils, which are prominent cells in asthmatic inflammation, undergo apoptosis and are recognized and engulfed by phagocytic macrophages in vitro. We have examined the ability of human small airway epithelial cells (SAEC) to recognize and ingest apoptotic human eosinophils, Cultured SAEC ingested apoptotic eosinophils but not freshly isolated eosinophils or opsonized erythrocytes. The ability of SAEC to ingest apoptotic eosinophils was enhanced by interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor alpha (TNF alpha) in a time- and concentration-dependent fashion. IL-1 alpha was found to be more potent than TNF alpha and each was optimal at 10(-10) mol/L, with a significant (P < .05) effect observed at 1 hour postcytokine incubation that was maximal at 5 hours. IL-1 alpha stimulation not only increased the number of SAEC engulfing apoptotic eosinophils, but also enhanced their capacity for ingestion. The amino sugars glucosamine, n-acetyl glucosamine, and galactosamine significantly inhibited uptake of apoptotic eosinophils by both resting and IL-1 alpha-stimulated SAEC, in contrast to the parent sugars glucose, galactose, mannose, and fucose. Incubation of apoptotic eosinophils with the tetrapeptide RGDS, but not RGES, significantly inhibited their uptake by both resting and IL-1 alpha-stimulated SAEC, as did monoclonal antibody against alpha v beta 3 and CD36. Thus, SAEC recognize apoptotic eosinophils via lectin- and integrin-dependent mechanisms. These data demonstrate a novel function for human bronchial epithelial cells that might represent an important mechanism in the resolution of eosinophil-induced asthmatic inflammation. (C) 1999 by The American Society of Hematology.",
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T1 - Resting and cytokine-stimulated human small airway epithelial cells recognize and engulf apoptotic eosinophils

AU - Walsh, G M

AU - Sexton, D W

AU - Blaylock, M G

AU - Convery, C M

PY - 1999

Y1 - 1999

N2 - Eosinophils, which are prominent cells in asthmatic inflammation, undergo apoptosis and are recognized and engulfed by phagocytic macrophages in vitro. We have examined the ability of human small airway epithelial cells (SAEC) to recognize and ingest apoptotic human eosinophils, Cultured SAEC ingested apoptotic eosinophils but not freshly isolated eosinophils or opsonized erythrocytes. The ability of SAEC to ingest apoptotic eosinophils was enhanced by interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor alpha (TNF alpha) in a time- and concentration-dependent fashion. IL-1 alpha was found to be more potent than TNF alpha and each was optimal at 10(-10) mol/L, with a significant (P < .05) effect observed at 1 hour postcytokine incubation that was maximal at 5 hours. IL-1 alpha stimulation not only increased the number of SAEC engulfing apoptotic eosinophils, but also enhanced their capacity for ingestion. The amino sugars glucosamine, n-acetyl glucosamine, and galactosamine significantly inhibited uptake of apoptotic eosinophils by both resting and IL-1 alpha-stimulated SAEC, in contrast to the parent sugars glucose, galactose, mannose, and fucose. Incubation of apoptotic eosinophils with the tetrapeptide RGDS, but not RGES, significantly inhibited their uptake by both resting and IL-1 alpha-stimulated SAEC, as did monoclonal antibody against alpha v beta 3 and CD36. Thus, SAEC recognize apoptotic eosinophils via lectin- and integrin-dependent mechanisms. These data demonstrate a novel function for human bronchial epithelial cells that might represent an important mechanism in the resolution of eosinophil-induced asthmatic inflammation. (C) 1999 by The American Society of Hematology.

AB - Eosinophils, which are prominent cells in asthmatic inflammation, undergo apoptosis and are recognized and engulfed by phagocytic macrophages in vitro. We have examined the ability of human small airway epithelial cells (SAEC) to recognize and ingest apoptotic human eosinophils, Cultured SAEC ingested apoptotic eosinophils but not freshly isolated eosinophils or opsonized erythrocytes. The ability of SAEC to ingest apoptotic eosinophils was enhanced by interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor alpha (TNF alpha) in a time- and concentration-dependent fashion. IL-1 alpha was found to be more potent than TNF alpha and each was optimal at 10(-10) mol/L, with a significant (P < .05) effect observed at 1 hour postcytokine incubation that was maximal at 5 hours. IL-1 alpha stimulation not only increased the number of SAEC engulfing apoptotic eosinophils, but also enhanced their capacity for ingestion. The amino sugars glucosamine, n-acetyl glucosamine, and galactosamine significantly inhibited uptake of apoptotic eosinophils by both resting and IL-1 alpha-stimulated SAEC, in contrast to the parent sugars glucose, galactose, mannose, and fucose. Incubation of apoptotic eosinophils with the tetrapeptide RGDS, but not RGES, significantly inhibited their uptake by both resting and IL-1 alpha-stimulated SAEC, as did monoclonal antibody against alpha v beta 3 and CD36. Thus, SAEC recognize apoptotic eosinophils via lectin- and integrin-dependent mechanisms. These data demonstrate a novel function for human bronchial epithelial cells that might represent an important mechanism in the resolution of eosinophil-induced asthmatic inflammation. (C) 1999 by The American Society of Hematology.

KW - VITRONECTIN RECEPTOR

KW - IN-VITRO

KW - MACROPHAGE RECOGNITION

KW - MONOCLONAL-ANTIBODIES

KW - MEDIATED PHAGOCYTOSIS

KW - DENDRITIC CELLS

KW - DEATH

KW - NEUTROPHILS

KW - PHOSPHATIDYLSERINE

KW - ASTHMA

M3 - Article

VL - 94

SP - 2827

EP - 2835

JO - Blood

JF - Blood

SN - 0006-4971

ER -