May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Immunomodulatory Role of VIP in a Murine Model of Pseudomonas aeruginosa–Induced Keratitis
Author Affiliations & Notes
  • E.A. Szliter
    Anatomy & Cell Biology, Wayne State Univ Sch of Med, Detroit, MI
  • S. Lighvani
    Anatomy & Cell Biology, Wayne State Univ Sch of Med, Detroit, MI
  • L.D. Hazlett
    Anatomy & Cell Biology, Wayne State Univ Sch of Med, Detroit, MI
  • Footnotes
    Commercial Relationships  E.A. Szliter, None; S. Lighvani, None; L.D. Hazlett, None.
  • Footnotes
    Support  NEI Grant R01EY02986 and P30EY04068
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 1922. doi:
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      E.A. Szliter, S. Lighvani, L.D. Hazlett; Immunomodulatory Role of VIP in a Murine Model of Pseudomonas aeruginosa–Induced Keratitis . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1922.

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

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Abstract

Purpose: : In Pseudomonas aeruginosa ocular infection, dominant T–helper cell 1 (Th1)–responsive mouse strains are susceptible (cornea perforates), while Th2–responsive mouse strains are resistant (cornea heals). Neuropeptides are endogenous neuroendocrine factors that have recently been correlated with neuroimmune interaction and function, but little is known of their role in mediating or regulating ocular infectious disease. Previous studies have shown an increased level of expression for vasoactive intestinal peptide (VIP), a neuropeptide associated with potent anti–inflammatory activities, in BALB/c (Th2–responder) vs. C57BL/6 (B6) (Th1–responder) mice. Therefore, the purpose of this study was to examine the role of VIP in modulating the host immune response to P. aeruginosa–induced keratitis.

Methods: : B6 mice were injected intraperitoneally with recombinant (r) VIP daily from –1 through 7 days p.i. Control mice were similarly injected with PBS. Clinical scores, slit–lamp, viable bacterial plate counts, myeloperoxidase (MPO) for PMN quantitation, multiprobe ribonuclease protection assays (RPA) and real–time RT–PCR were used to assess the effects of rVIP treatment in modulating disease pathogenesis.

Results: : Injection of B6 mice with rVIP prevented corneal perforation, normally seen in the susceptible animal by 5–7 days p.i. Real–time RT–PCR analysis of rVIP versus control corneas showed significantly decreased levels for IFN–γ, IL–1ß, MIP–2 and TNF–α mRNA at 7 days p.i. Bacterial load remained comparable for rVIP versus control animals, while PMN infiltration appeared more controlled upon rVIP treatment.

Conclusions: : These data provide evidence that VIP is a regulatory molecule of ocular inflammation. rVIP treatment counterbalanced the production of pro–inflammatory cytokines, IFN–γ and IL–1ß, and regulated PMN infiltration sufficiently to ameliorate the host–induced component of bacterial–induced inflammatory disease.

Keywords: cornea: basic science • bacterial disease • immunomodulation/immunoregulation 
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