April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Potential autocrine regulation of interleukin-33/ST2 signaling of corneal epithelium in Fungal Keratitis
Author Affiliations & Notes
  • Jing Lin
    Ophthalmology, the Affiliated Hospital of Qingdao Medical College,Qingdao University, Qingdao, China
  • Guiqiu Zhao
    Ophthalmology, the Affiliated Hospital of Qingdao Medical College,Qingdao University, Qingdao, China
  • Liting Hu
    Ophthalmology, the Affiliated Hospital of Qingdao Medical College,Qingdao University, Qingdao, China
  • Chengye Che
    Ophthalmology, the Affiliated Hospital of Qingdao Medical College,Qingdao University, Qingdao, China
  • Nan Jiang
    Ophthalmology, the Affiliated Hospital of Qingdao Medical College,Qingdao University, Qingdao, China
  • Footnotes
    Commercial Relationships Jing Lin, None; Guiqiu Zhao, None; Liting Hu, None; Chengye Che, None; Nan Jiang, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 6276. doi:
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    • Get Citation

      Jing Lin, Guiqiu Zhao, Liting Hu, Chengye Che, Nan Jiang, ; Potential autocrine regulation of interleukin-33/ST2 signaling of corneal epithelium in Fungal Keratitis. Invest. Ophthalmol. Vis. Sci. 2014;55(13):6276.

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

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Abstract

Purpose: Corneal innate immune responses are key mediators of the host’s defense against microbial infection, including fungal keratitis. Interleukin (IL) 33 is well known to promote Th2 type immune responses by signaling through its receptor ST2. However, it is not clear how ST2 responds to IL-33 to induce pro-inflammatory mediator in fungal keratitis. This study was to explore the role of IL-33/ST2 signaling in regulating the pro- inflammatory cytokine production in fungal keratitis and its role in the innate immune response triggered by inactive Af conidia.

Methods: Telomerase-immortaliz

Results: In ex vivo donor normal corneal epithelium, IL-33 protein was detected to be located in basal layers and ST2 protein was detected to be located in superficial layers, both of them were stimulated to multiple layers of the epithelium exposed to Af conidia. Af conidia significantly stimulated production of pro- inflammatory cytokines (IL-33, IL-6, IL-1β) by TCECs at both mRNA and protein levels. These stimulated production of pro-inflammatory mediators by Af conidia was blocked by soluble ST2 protein and was stimulated by IL-33. Interestingly, p38 MAPK inhibitor SB203580 also suppressed the production of these pro-inflammatory cytokines induced by Af conidia.

Conclusions: These findings demonstrate that IL-33/ST2 signaling plays an important role in fungal keratitis and it contributes to the innate immune responses triggered by inactive conidia by induction of pro-inflammatory cytokines such as IL-6 and IL-1β through the p38 MAPK pathway, and suggesting a molecular mechanism by which local allergic inflammatory response may be amplified by corneal epithelial cell produced IL-33 through potential autocrine regulation.

Keywords: 482 cornea: epithelium • 530 fungal disease  
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