Open AccessRole of nitric oxide in Sjögren's syndrome
Author(s) -
Konttinen Yrjö T.,
Platts Louise A. M.,
Tuominen Susanne,
Eklund Kari K.,
Santavirta Nina,
Törnwall Jyrki,
Sorsa Timo,
Hukkanen Mika,
Polak Julia M.
Publication year - 1997
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780400515
Subject(s) - nitric oxide , sjögren syndrome , medicine , immunopathology , dermatology , systemic disease
Objective. To measure levels of salivary nitrite (NO 2 ‐ ) and to localize nitric oxide synthases (NOS) in the labial salivary glands (LSGs) of patients with Sjögren's syndrome (SS). Methods. NO 2 ‐ was measured by the Griess reaction. LSGs were analyzed using NADPH‐diaphorase histochemical and immunohistochemical studies to determine the constitutive NOS (neuronal [ncNOS] and endothelial [ecNOS]) and inducible NOS (iNOS) isoforms. Results. The NO 2 ‐ concentration (mean ± SEM 307 ± 51 μ M versus 97 ± 16 μ M ; P < 0.05) and output (166 ± 46 nmoles/minute versus 37 ± 7 nmoles/minute) were increased in SS patients compared with healthy control subjects. NADPH‐diaphorase was found in some nerve fibers and endothelial cells, and, in SS, was found in myoepithelial, acinar, and ductal epithelial cells, but in only a few inflammatory cells. In SS, ncNOS‐immunoreactive nerve fibers were sparse and ecNOS was found in a minority of the CD31‐positive vascular endothelial cells and acinar cells, whereas iNOS was localized in myoepithelial, acinar, and ductal epithelial cells, often together with tumor necrosis factor α. Conclusion. Nitrite was found in normal human saliva. NO produced by ncNOS probably acts as a non‐adrenergic, noncholinergic neurotransmitter, whereas that produced by ecNOS exerts a vasodilatory effect. SS patients had increased NO 2 ‐ concentrations, with most of the superfluous salivary NO being produced not by the immigrant inflammatory cells, but rather, by the resident salivary gland cells. NO may contribute to inflammatory damage and acinar cell atrophy in SS.