Emerging avenues linking inflammation, angiogenesis and Sjögren’s syndrome

► The salivary epithelial cells perpetuate chronic inflammation in Sjögren’s syndrome. ► Sjögren’s syndrome is characterized by the overexpression of inflammatory cytokines. ► Angiogenesis and inflammation are mutually correlated. ► Neovascularization contributes to the perpetuation of inflammation....

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Published in:Cytokine (Philadelphia, Pa.) Pa.), 2013-03, Vol.61 (3), p.693-703
Main Authors: Lisi, Sabrina, Sisto, Margherita, D’Amore, Massimo, Lofrumento, Dario Domenico, Ribatti, Domenico
Format: Article
Language:English
Subjects:
angiogenesis
Animals
antigen presentation
apoptosis
autoimmune diseases
chemokines
Chronic Disease
Chronic inflammation
epithelial cells
etiology
Humans
inflammation
Inflammation - complications
Inflammation - pathology
Inflammation Mediators - metabolism
IκBα
Neovascularization
Neovascularization, Pathologic - complications
Neovascularization, Pathologic - pathology
NF-κB
pathogenesis
pathophysiology
Salivary glands
Signal Transduction
Sjogren's Syndrome - complications
Sjogren's Syndrome - immunology
Sjogren's Syndrome - pathology
Sjogren's Syndrome - therapy
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Summary:► The salivary epithelial cells perpetuate chronic inflammation in Sjögren’s syndrome. ► Sjögren’s syndrome is characterized by the overexpression of inflammatory cytokines. ► Angiogenesis and inflammation are mutually correlated. ► Neovascularization contributes to the perpetuation of inflammation. ► The production of angiogenic factors occurs via NF-κB activation. Sjögren’s syndrome (SS) is an autoimmune disease characterized by an inflammatory mononuclear infiltration and the destruction of epithelial cells of the lachrymal and salivary glands. The aetiology is unknown. The expression “autoimmune epithelitis” has been proposed as an alternative to SS, in view of the emerging central role of the epithelial cells in the disease pathogenesis. At the biomolecular level, the epithelial cells play an important role in triggering the autoimmune condition via antigen presentation, apoptosis, and chemokine and cytokines release. Inflammation and angiogenesis are frequently coupled in the pathological conditions associated to autoimmune diseases, and an angiogenic imbalance contributes to the pathogenesis of a number of inflammatory disorders. This work reviews the current knowledge of the molecular and cellular mechanisms underlying the pathogenesis of the inflammatory reactions that characterize SS. The literature and our data on the role of angiogenesis in the pathophysiology of the disease are discussed.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2012.12.021