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Intravitreal Injection and Quantitation of Infection Parameters in a Mouse Model of Bacterial Endophthalmitis
Published on: February 6, 2021
Vasoactive intestinal peptide (VIP) exacerbates endotoxin-induced uveitis (EIU) in mice
1Laboratory of Immunology, National Eye Institute, NIH, Bethesda, Maryland, United States of America. zhangm@intra.nei.nih.gov
Current Eye Research
|March 23, 2001
Summary
Vasoactive intestinal peptide (VIP) worsens experimental autoimmune uveitis (EIU) by reducing tumor necrosis factor-alpha (TNF-alpha), confirming that lower TNF-alpha levels paradoxically increase EIU severity.
Area of Science:
- Immunology
- Neuroendocrinology
- Ophthalmology
Background:
- Tumor necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine.
- Inhibition of TNF-alpha has been shown to exacerbate experimental autoimmune uveitis (EIU).
- Vasoactive intestinal peptide (VIP) is a neuropeptide that inhibits TNF-alpha production.
Purpose of the Study:
- To investigate the effect of VIP on EIU.
- To further understand the paradoxical relationship between TNF-alpha and EIU.
Main Methods:
- VIP was administered concurrently with endotoxin in mice to induce EIU or lethality.
- EIU severity was assessed by counting infiltrating cells in eye sections.
- Serum levels of TNF-alpha, IL-1beta, and IL-10 were measured.
Main Results:
- VIP administration exacerbated EIU.
- VIP treatment provided partial protection against endotoxin-induced lethality.
- VIP reduced serum levels of TNF-alpha and IL-1beta, but increased IL-10 levels.
Conclusions:
- This study reinforces the paradoxical finding that reducing circulating pro-inflammatory cytokines, specifically TNF-alpha, exacerbates EIU.
- VIP's effect on EIU highlights a complex interplay between neuropeptides and inflammatory responses in the eye.
