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Blood, Vol. 94 No. 8 (October 15), 1999:
pp. 2827-2835
Resting and Cytokine-Stimulated Human Small Airway Epithelial Cells
Recognize and Engulf Apoptotic Eosinophils
Garry M. Walsh,
Darren W. Sexton,
Morgan G. Blaylock, and
Catherine M. Convery
From the Department of Medicine & Therapeutics, University of
Aberdeen Medical School, Aberdeen, UK.
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
(IL-1) or tumor necrosis factor (TNF) in a time- and
concentration-dependent fashion. IL-1 was found to be more potent
than TNF 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
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-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-stimulated SAEC, as did monoclonal
antibody against v 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.
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