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Ex Vivo Organotypic Corneal Model of Acute Epithelial Herpes Simplex Virus Type I Infection
Published on: November 3, 2012
[Cytokine expression in murine cornea tissue during recurrent herpetic stromal keratitis]
Li-kun Xia1, Jin-song Zhang, Xiao-long Chen
1Department of Ophthalmology, The Second Affiliated Hospital, China Medical University, Shenyang 110004, China. xialk@online.ln.cn
Insights
Recurrent herpetic stromal keratitis (HSK) involves both Th1 and Th2 cytokines, with IFN-gamma and IL-10 expression correlating with corneal inflammation severity. This suggests a complex immune response to HSV-1 reactivation.
Area of Science:
- Immunology
- Ophthalmology
- Virology
Context:
- Herpetic stromal keratitis (HSK) is a significant cause of vision loss.
- Recurrent HSK is driven by herpes simplex virus type 1 (HSV-1) reactivation.
- Understanding the immune response in HSK is crucial for developing effective treatments.
Purpose:
- To investigate the expression of T helper type 1 (Th1) and T helper type 2 (Th2) cytokines in the murine cornea during recurrent HSK.
- To determine the relationship between cytokine expression and the severity of HSK.
Summary:
- Both Th1 (IFN-gamma, IL-12) and Th2 (IL-4, IL-10) cytokines were expressed during recurrent HSK in mice.
- IFN-gamma and IL-10 mRNA levels correlated with the degree of corneal opacification.
- IL-12 p40 was detected early after viral reactivation, while IL-4 increased during inflammation.
Impact:
- The findings suggest that recurrent HSK involves a mixed Th1/Th2 immune response.
- The balance between pro-inflammatory and regulatory cytokines may influence corneal tissue damage and repair.
- This research provides insights into the immunopathogenesis of HSK, potentially guiding therapeutic strategies.
Objective:
To investigate the expression of cytokine in CD(4)(+) T helper type 1 (Th1) and T helper type 2 (Th2) cells in murine cornea during recurrent herpetic stromal keratitis (HSK) and its relationship with the HSK.
Methods:
Seven weeks after corneal inoculation with HSV-1, the eyes of latently infected BALB/c mice were irradiated by UV-B and examined for the signs of inflammation and viral reactivation. The corneas of six mice with recurrent stromal disease and six controls were examined to detect the content of Th1 type cytokines (IFN-gamma and IL-12) and Th2 type cytokines (IL-4 and IL-10) on days 0, 3, 7, 10, 14, 21 and 28 after irradiation.
Results:
Peak of the inflammation process of HSK, manifested by stromal opacification, occurred 7-14 days after viral reactivation in latently infected mice. In semi-quantitative RT-PCR analyses, IFN-gamma, IL-12 p40, IL-10 and IL-4 mRNA were expressed before and during the clinical course of recurrent HSK. The highest expression of IFN-gamma and IL-10 was revealed during the occurrence and development of corneal inflammation (3 -14 days after the reactivation of virus) with a decline at the recovering process (after 14 days). The expression of IFN-gamma and IL-10 was co-related with the degree of corneal opacification. Large amounts of IL-12 p40 mRNA were detected in the cornea 3 days after the virus reactivation and maintained over the whole course of observation. IL-4 levels increased at 3-14 days after the reactivation of virus and declined after day 14.
Conclusions:
Th1 and Th2 cytokines present together throughout the course of the inflammatory process accompanying recurrent corneal HSV-1 infection, which is likely associated with a memory response to viral antigens. The expression of IL-10 mRNA parallels with the expression of IFN-gamma and is co-related with the degree of corneal inflammation. The damage and repair of corneal tissue in recurrent HSK may depend upon the balance between the destructive cytokines and protective cytokines at the site of virus reactivation.
