4.3 Article

Role of Dectin-1 in the innate immune response of rat corneal epithelial cells to Aspergillus fumigatus

Journal

BMC OPHTHALMOLOGY
Volume 15, Issue -, Pages -

Publisher

BIOMED CENTRAL LTD
DOI: 10.1186/s12886-015-0112-1

Keywords

Dectin-1; Innate immune; Corneal epithelium; Rat fungal keratitis; Laminarin

Categories

Funding

  1. National Natural Science Foundation of China [81170825, 81470609]
  2. Shandong province natural science foundation [ZR2013HQ007, ZR2012HZ001]
  3. Specialized Research Fund for the Doctoral Program of Higher Education [20123706110003]

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Background: To observe Dectin-1 expression in fungal keratitis on rat models and to determine the role of Dectin-1 in innate immune response to Aspergillus fumigatus. Methods: Wistar rats were randomly divided into control, fungal keratitis and pretreatment (pretreated with Laminarin) groups. Samples were used for conducting immunohistochemical staining and real-time PCR to observe expression of cytokines like CCL2, CCL3, CXCL1, CXCL2, IL-1 beta, TNF-alpha, IL-6, IL-10. Results: After fungal stimulations, all 7 inflammatory factors, except IL-10, increased with different levels. After 4 h of fungal stimulations, IL-1 beta, IL-6, CCL2, CXCL1 and CXCL2 of pretreatment groups were significantly (p < 0.05) lower than fungal groups, while the other 3 cytokines had no significant changes. After 8 h of fungal stimulations, IL-6 and CXCL1 of pretreatment groups were still significantly (p < 0.05) lower than fungal groups. Discussion: With progress of fungus stimulation, expression of IL-1 beta, CXCL1, CXCL2, MCP-1 gradually increased, whilepretreated with Laminarin to block Dectin-1, these expression decreased, indicating that Dectin-1 maypromote immune reaction through them. IL-10 decreased in fungal group because of itsimmunosuppressive effect at 4h, and it began to increase at 8h to suppress Th1 inflammation response inorder to avoid excessive tissue damage. Conclusion: Dectin-1 in early period of innate immune responses in rat fungal keratitis might work through IL-1 beta, IL-6, CCL2, CXCL1, CXCL2 to recruit neutrophils and macrophages to participate anti-fungal immunity.

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