ArticleScientific reports2017
Functional effects of proinflammatory factors present in Sjögren's syndrome salivary microenvironment in an in vitro model of human salivary gland.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- IFN-γ-Associated Signaling Networks in Interstitial Lung Disease Associated With Sjögren's Disease.Immunity, inflammation and disease · 2026Review
- Distinct molecular profile in Sjögren's syndrome is associated with disease activity and clinical manifestations.Scientific reports · 2026Article
- Alterations in histology of the aging salivary gland and correlation with the glandular inflammatory microenvironment.iScience · 2023Article
- Genome-wide association study identifies Sjögren's risk loci with functional implications in immune and glandular cells.Nature communications · 2022Article
- In vitro effects of curcumin on proinflammatory cytokines and expression of their genes in minor salivary gland tissue of patients with Sjogren's syndrome.Rheumatology international · 2022Article
- Inflammatory Stratification in Primary Sjögren's Syndrome Reveals Novel Immune Cell Alterations in Patients' Minor Salivary Glands.Frontiers in immunology · 2021Article
- Current State of Knowledge on Primary Sjögren's Syndrome, an Autoimmune Exocrinopathy.Journal of clinical medicine · 2020Review
- Insight into Salivary Gland Aquaporins.Cells · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary Sjögren's syndrome (pSS) is an autoimmune exocrinopathy in which the role that the immune response plays in reducing exocrine gland function, including the glandular microenvironment of cytokines, has not been fully understood. Epithelial cells from biopsies of human parotid gland (HPG) were used to establish a model of human salivary gland in vitro. In this model, the functional consequences of several proinflammatory soluble factors present in the pSS glandular microenvironment were assessed. Stimulation with isoproterenol and calcium produced a significant increase in the basal activity of amylase in the HPG cell supernatants. Under these conditions, the presence of TNF-α and CXCL12 increased amylase mRNA cellular abundance, but reduced the amylase activity in the cell-free supernatant in a dose-dependent manner. IL-1β and IFN-γ, but not TGF-β, also diminished amylase secretion by HPG cells. These results suggest that the glandular microenvironment of cytokine, by acting post-transcriptionally, may be responsible, at least in part, for the reduced exocrine function observed in pSS patients. These data may help to a better understanding of the pathogenesis of SS, which in turn would facilitate the identification of new therapeutic targets for this disorder.
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