September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Tumor necrosis factor-α-inducible protein 2 is indispensable for host defense against Candida albicans keratitis
Author Affiliations & Notes
  • Bing Xu
    Anatomy and Cell Biology and Ophthalmology, Wayne State University School of Medicine, Detroit, Michigan, United States
  • Nan Gao
    Anatomy and Cell Biology and Ophthalmology, Wayne State University School of Medicine, Detroit, Michigan, United States
  • Fushin X Yu
    Anatomy and Cell Biology and Ophthalmology, Wayne State University School of Medicine, Detroit, Michigan, United States
  • Footnotes
    Commercial Relationships   Bing Xu, None; Nan Gao, None; Fushin Yu, None
  • Footnotes
    Support  NIH/NEI EY017960
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 324. doi:
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    • Get Citation

      Bing Xu, Nan Gao, Fushin X Yu; Tumor necrosis factor-α-inducible protein 2 is indispensable for host defense against Candida albicans keratitis. Invest. Ophthalmol. Vis. Sci. 2016;57(12):324.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Tumor necrosis factor-α-inducible protein 2 (TNFAIP2) was first identified as a TNF-α-regulated gene in human endothelial cells and was found to be highly expressed in malignant tumor cells. However, rarely has the role of TNFAIP2 been characterized in infection. Our study aims to investigate the expression and functions of TNFAIP2 in a mouse model of Candida albicans (CA) keratitis.

Methods : C57BL/6 mouse corneas were scratched and pretreated with 500ng flagellin for 24h. Then mouse corneas were re-scratched and inoculated with 1.0X105 CFUs of CA. Mouse epithelial cells or whole corneas were collected at indicated time points for PCR and western blot analysis. The functions of TNFAIP2 in CA keratitis was assessed by subconjunctival injection of TNFAIP2 siRNA. Viable fungal load was determined by direct plate counts.

Results : TNFAIP2 transcripts were detected in mouse corneal epithelial cells as early as 6 hour post infection (hpi). Flagellin pretreatment not only alleviated the infection, but also reduced the mRNA expression of TNFAIP2. CA infection induced TNFAIP2 protein expression at 18 hpi in both corneal epithelial cells and in the whole corneal extracts. Silencing of TNFAIP2 by application of siRNA increased the severity of keratitis, comparing with scramble siRNA control. In addition, silencing of TNFAIP2 increased the fungal burden in mouse corneas.

Conclusions : These data demonstrate that TNFAIP2 is an indispensable cytokine in host defense against CA infection, indicating TNFAIP2 may be a potential therapeutic agent for the treatment of infectious keratitis.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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