期刊
CORNEA
卷 35, 期 2, 页码 267-273出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/ICO.0000000000000710
关键词
mannose receptor; corneal epithelial cells; Aspergillus fumigatus; innate immunity; dectin-1
资金
- National Natural Science Foundation of China [81470609, 81170825]
- Natural Science Foundation of Shandong Province [ZR2013HQ007, ZR2012FZ001]
- Specialized Research Fund for the Doctoral Program of Higher Education [20123706110003]
Purpose:To investigate the expression and function of the mannose receptor (MR) and to explore its interaction with dectin-1 in human corneal epithelial cells (HCECs) exposed to Aspergillus fumigatus.Methods:HCECs were stimulated with A. fumigatus for 0, 4, 8, 12, 16, and 24 hours. MR expression was tested by the polymerase chain reaction, Western blot, and immunohistochemistry. HCECs were pretreated with 2 g/mL MR-blocking antibody. The expressions of p38, phosphorylated p38 (p-p38), and the downstream cytokines (TNF- and IL-1) and dectin-1 were tested by the polymerase chain reaction, Western blot, and enzyme-linked immunosorbent assay. HCECs were pretreated with dectin-1 agonists (curdlan, 100 g/mL) and inhibitors (laminarin, 10 g/mL), and the expression of the MR was tested.Results:MR expression was upregulated after stimulation with A. fumigatus. MR mRNA and protein levels began to rise at 8 and 16 hours, respectively. Stronger immunostaining of the MR was observed in fungal-infected corneal epithelium than in normal corneal epithelium. Aspergillus fumigatus increased the production of TNF- (11-fold, 4-fold of the control), IL-1 (4.7-fold, 3-fold of the control), p-p38 (2.1-fold of the control), and dectin-1 (2.3-fold, 2-fold of the control) in mRNA and protein levels. The MR antibody significantly suppressed the expression of TNF- (28%, 50% reduction), IL-1 (38%, 42% reduction), p-p38 (38% reduction), and dectin-1 (48%, 47% reduction). Curdlan increased the production of the MR (1.5-fold, 1.9-fold of the control), whereas laminarin decreased the expression of the MR (50%, 60% reduction) induced by A. fumigatus.Conclusions:HCECs express the MR, and A. fumigatus infection can increase MR expression. A. fumigatus induces the expression of inflammatory cytokines through the MR and p38 MAPK pathway. The expression of dectin-1 and the MR had mutual influence.
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