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Published on: May 30, 2018
Corneal transcriptomic signatures of mycotoxin exposure reveal distinct immune and metabolic responses
Xiaoyuan Sha1, Junjie Tang2, Yahong Li3
1Department of Ophthalmology, The Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan 523000, China; Department of Ophthalmology, The First Affiliated Hospital of Jinan University, Jinan University, Guangzhou 510630, China.
Abstract:
Fungal keratitis (FK) is a vision-threatening infection in which Fusarium species not only invade the cornea but may also release mycotoxins that exacerbate tissue injury. Here, we established a corneal exposure model to delineate the direct effects of Fusarium-derived mycotoxins independent of live fungal infection, using deoxynivalenol (DON), fumonisin B1 (FB1), and T-2 toxin as representative compounds. Hstological analyses revealed that all three mycotoxins markedly impaired corneal epithelial repair, induced stromal disorganization, and promoted inflammatory cell infiltration. At the molecular level, toxin exposure consistently activated immune-related pathways, including cytokine-cytokine receptor interaction, chemokine signaling, and IL-17 signaling, while concurrently suppressing metabolic and detoxification pathways such as cytochrome P450-mediated drug and xenobiotic metabolism. Despite these shared pathogenic features, each mycotoxin exhibited specific regulatory signatures, with T-2 toxin inducing the most pronounced transcriptomic disruption. These findings demonstrate that Fusarium mycotoxins are sufficient to drive corneal inflammation and tissue damage, providing mechanistic insight into mycotoxin-associated corneal injury.
Insights
Fusarium fungal keratitis (FK) involves mycotoxins damaging the cornea. These toxins impair healing, cause inflammation, and disrupt corneal cell pathways, leading to vision-threatening injury.
Area of Science:
- Ophthalmology
- Mycology
- Toxicology
Background:
- Fungal keratitis (FK) is a serious eye infection caused by Fusarium species.
- Fusarium species can release mycotoxins that worsen corneal damage.
- The direct impact of these mycotoxins on corneal injury is not fully understood.
Purpose of the Study:
- To investigate the direct effects of Fusarium-derived mycotoxins on corneal tissue.
- To analyze the molecular and histological changes induced by specific mycotoxins.
- To understand the role of mycotoxins in Fusarium-associated corneal pathology.
Main Methods:
- Established a corneal exposure model using deoxynivalenol (DON), fumonisin B1 (FB1), and T-2 toxin.
- Performed histological analyses to assess tissue damage and repair.
- Conducted molecular analyses to identify affected cellular pathways.
Main Results:
- All tested mycotoxins impaired corneal epithelial repair and promoted inflammation.
- Mycotoxin exposure activated immune pathways (cytokine-cytokine receptor, chemokine, IL-17 signaling).
- Metabolic and detoxification pathways (cytochrome P450) were suppressed; T-2 toxin caused the most disruption.
Conclusions:
- Fusarium mycotoxins are sufficient to cause corneal inflammation and damage independently of live fungal infection.
- Mycotoxins contribute significantly to the pathogenesis of fungal keratitis.
- This study provides mechanistic insights into mycotoxin-induced corneal injury.
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