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Porcine Corneal Tissue Explant to Study the Efficacy of Herpes Simplex Virus-1 Antivirals
Published on: September 20, 2021
Polluted Air Exposure Compromises Corneal Immunity and Exacerbates Inflammation in Acute Herpes Simplex Keratitis
Victor G Sendra1, Julia Tau1, Gustavo Zapata1
1Laboratorio Traslacional de Inmunopatología y Oftalmología, Departamento de Patología, Facultad de Medicina, Universidad de Buenos Aires, Cuidad Autónoma de Buenos Aires, Argentina.
Urban air pollution worsens herpes simplex keratitis (HSK) severity by increasing inflammation and immune cell activity in the eye. This study highlights air pollution as a critical factor in ocular inflammatory diseases.
Area of Science:
- Environmental Science
- Immunology
- Ophthalmology
Background:
- Air pollution is a global environmental concern, particularly in megacities, impacting public health and exacerbating ocular diseases.
- Herpes simplex keratitis (HSK), caused by herpes simplex virus type 1 (HSV-1), can lead to corneal scarring and vision impairment.
Purpose of the Study:
- To investigate the immunopathological effects of urban air pollution on acute herpes simplex keratitis (HSK).
- To model HSK in mice exposed to experimental urban polluted air from Buenos Aires.
Main Methods:
- Evaluated clinical outcomes, viral DNA, and pro-inflammatory cytokines (TNF-α, IL-1β, IFN-γ, CCL2) using RT-PCR and ELISA.
- Assessed innate and adaptive immune responses in the cornea and lymph nodes via immunofluorescence and flow cytometry.
Main Results:
- Polluted air exposure led to more severe HSK, with increased corneal opacity, neovascularization, and viral DNA.
- Elevated pro-inflammatory cytokines and a significant influx of immune cells (neutrophils, monocytes, dendritic cells, T cells) were observed in the cornea.
- A shift towards a Th1 immune response over regulatory T cells (Tregs) in lymph nodes, with decreased corneal Tregs, was noted.
Conclusions:
- Urban air pollution exacerbates HSK severity by disrupting local immune responses.
- Air pollution acts as a key factor in the development and progression of ocular inflammatory diseases.
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