Abstract
Professional phagocytes such as dendritic cells and macrophages can ingest particles larger than 0.5 μm in diameter. Epithelial cells are nonprofessional phagocytes that cannot ingest pathogenic microorganisms, but they can ingest apoptotic cells. Inhibition of the engulfment of apoptotic cells by the airway epithelium can cause severe airway inflammation. Vascular endothelial growth factor (VEGF) is an angiogenesis-promoting factor that can mediate allergic airway inflammation and can promote airway epithelial cells (AECs) proliferation, but it is not clear whether it affects the engulfment of apoptotic cells by AECs. In the present study, VEGF inhibited engulfment of apoptotic cells by AECs via binding to VEGF receptor(R)2. This inhibitory effect of VEGF was not influenced by masking of phosphatidylserine (PS) on the surface of apoptotic cells and was partially mediated by the PI3K-Akt signaling pathway. VEGF inhibition of phagocytosis involved polymerization of actin and downregulation of the expression of the phagocytic-associated protein Beclin-1 in AECs. Since engulfment of apoptotic cells by AECs is an important mechanism for airway inflammation regression, VEGF inhibition of the engulfment of apoptotic cells by airway epithelial cells may be important for mediating allergic airway inflammation.
Highlights
Phagocytic cells can engulf particles larger than 0.5 μm in diameter [1]
The morphology of cultured primary airway epithelial cells (AECs) was not changed by 500 ng/ml Vascular endothelial growth factor (VEGF)
As shown in (Figure 1(c)), 300, 500, and 1000 ng/ml VEGF significantly inhibited the phagocytosis of apoptotic cells, with the greatest inhibition caused by 500 ng/ml
Summary
Specialized or professional phagocytes like dendritic cells (DCs) and macrophages play an important role in the resistance to infection by pathogenic microbes and maintaining homeostasis. Nonprofessional phagocytes including epithelial cells and fibroblasts cannot phagocytize pathogenic microorganisms but can ingest apoptotic cells, a process known as efferocytosis [2, 3]. Programmed cell death, is a key process in tissue homeostasis, and phagocytosis of apoptotic cells by the tissue epithelium protects against inflammatory or immunogenic responses to the dying cells [4]. A recent study by Juncadella et al found that phagocytosis of apoptotic airway cells depended on. Ras-related C3 botulinum toxin substrate 1 (Rac1), which is a GTPase, and that defective phagocytosis contributed to allergic airway inflammation [5].
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