Phagocytosis of apoptotic eosinophils but not neutrophils by bronchial epithelial cells.
BACKGROUND
We have previously demonstrated that human bronchial epithelial cells engulf apoptotic eosinophils.


OBJECTIVE
To compare and contrast the phagocytic capabilities of monocyte-derived macrophage and primary airway epithelial cells for apoptotic granulocytes.


RESULTS
Here we compared phagocytosis of human apoptotic eosinophils and neutrophils by small and large airway epithelial cells (SAEC and LAEC) and monocyte-derived macrophages. Confocal microscopy of F-actin staining and scanning and transmission electron microscopy revealed phagocytic cup formation around apoptotic eosinophils by airway epithelial cells (AEC) membranes with evidence of their digestion. Resting and cytokine-stimulated AEC did not recognize and ingest apoptotic neutrophils. The latter were phagocytosed by macrophages that exhibited greater ingestion of and higher capacity for, apoptotic eosinophils over apoptotic neutrophils. Cytochalasin D completely abolished uptake of apoptotic eosinophils by SAEC, LAEC or macrophage monolayers. Ligation of epithelial cell CD44 receptors for 24 h increased phagocytosis of apoptotic eosinophils by SAEC and LAEC with a potency comparable with that of IL-1. Phagocytosis was a specific receptor-mediated process involving integrin- (alphavbeta3, alphavbeta5, CD36), phosphatidylserine receptor- and lectin-dependent mechanisms. No significant differences were observed in avarice for apoptotic eosinophils by SAEC or LAEC either resting, CD44 monoclonal antibodies- or cytokine- stimulated, or in their usage and expression of recognition receptors.


CONCLUSIONS
These findings further suggest and define an important role for the bronchial epithelium in the selective removal of apoptotic eosinophils from the airways in asthma.
Sexton
D W
DW
Department of Medicine and Therapeutics, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK.
Al-Rabia
M
M
Blaylock
M G
MG
Walsh
G M
GM
D017209:Apoptosis / Q000502:physiology*; D001980:Bronchi / Q000276:immunology / Q000502:physiology*; D002478:Cells, Cultured; D004804:Eosinophils / Q000502:physiology*; D004847:Epithelial Cells / Q000276:immunology / Q000502:physiology; D006801:Humans; D018960:Hyaluronan Receptors / Q000276:immunology; D016023:Integrins / Q000502:physiology; D007375:Interleukin-1 / Q000276:immunology; D056484:Jumonji Domain-Containing Histone Demethylases; D037102:Lectins / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D018613:Microscopy, Confocal / Q000379:methods; D008854:Microscopy, Electron / Q000379:methods; D008855:Microscopy, Electron, Scanning / Q000379:methods; D009504:Neutrophils / Q000502:physiology*; D010587:Phagocytosis / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000502:physiology
D018960:Hyaluronan Receptors; D016023:Integrins; D007375:Interleukin-1; D037102:Lectins; D011956:Receptors, Cell Surface; C408123:phosphatidylserine receptor; C498707:JMJD6 protein, human; D056484:Jumonji Domain-Containing Histone Demethylases