Format

Send to

Choose Destination
See comment in PubMed Commons below
Invest Ophthalmol Vis Sci. 1997 Sep;38(10):2161-4.

Increased plasma levels of substance P in vernal keratoconjunctivitis.

Author information

1
Institute of Neurobiology, National Research Council, and Department of Ophthalmology, University of Rome Tor Vergata, Italy.

Abstract

PURPOSE:

The increase of nerve growth factor (NGF) plasma levels in vernal keratoconjunctivitis (VKC) patients has been demonstrated previously. Results of numerous studies in vitro and in vivo have shown that NGF modulates the synthesis of substance P (SP), a neuropeptide involved in the pathogenesis of human allergic diseases. In this study the involvement of SP in this allergic conjunctivitis is investigated, along with its relationship with NGF and other systemic and local markers of VKC.

METHODS:

Competitive radioimmunoassays were used to detect the levels of SP in plasma, the levels of eosinophil cationic protein, and the total and specific immunoglobulin E in the serum of 11 patients with VKC and in 11 healthy matched controls. Plasma levels of nerve growth factor (NGF) were measured in all VKC patients and controls using an immunoenzymatic assay. Histologic evaluation was performed in tarsal and bulbar conjunctival specimens obtained in biopsies from 8 VKC patients and 4 control subjects.

RESULTS:

Patients with VKC show a significant increase of SP and NGF plasma levels (P < 0.003 and P < 0.001, respectively), and an increase of eosinophil cationic protein and immunoglobulin E levels in the serum (P < 0.001 and P < 0.002, respectively). Mast cells, eosinophils, and lymphocytes were also significantly increased in the conjunctiva of VKC patients. Interestingly enough, VKC patients with the highest NGF plasma levels also showed the highest SP levels.

CONCLUSIONS:

The data show the involvement of SP in VKC and suggest that SP with NGF could modulate the allergic response in this disease, probably through an interaction with inflammatory cytokines.

PMID:
9331280
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Silverchair Information Systems
    Loading ...
    Support Center