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Contribution of ductal cells to cytokine responses by human pancreatic islets
- Source :
- Vrije Universiteit Brussel
- Publication Year :
- 1999
-
Abstract
- In type 1 diabetes, autoimmune destruction of pancreatic beta-cells has been attributed to cytokines released from infiltrating immunocytes. Exposure of isolated islets to cytokines leads to nitric oxide (NO) production, which can damage beta-cells. Because ductal cells are closely associated with human beta-cells, we examined whether they can contribute to this process. Isolated human ductal cells were cultured for 48 h with various cytokines. The combination of interleukin-1beta (IL-1beta) plus interferon-gamma (IFN-gamma) increased nitric oxide production 12-fold while stimulating mRNA expression of inducible nitric oxide synthase (iNOS). In this condition, 10-20% of cells positive for the cytokeratin-19 duct marker also stained positive for iNOS protein, whereas no positive cells were found in control preparations. Comparison of the magnitude of iNOS mRNA expression and nitric oxide production in these cells with that in isolated human islets suggests that >50% of total islet nitric oxide production might originate from associated ductal cells. It is concluded that ductal cells are a potential source of nitric oxide production in human islets infiltrated by cytokine-releasing immunocytes.
- Subjects :
- Adult
medicine.medical_specialty
Adolescent
Ductal cells
Endocrinology, Diabetes and Metabolism
medicine.medical_treatment
Nitric Oxide Synthase Type II
Enteroendocrine cell
Nitric Oxide
Nitric oxide
chemistry.chemical_compound
Islets of Langerhans
Internal medicine
Gene expression
Internal Medicine
medicine
Humans
RNA, Messenger
Cells, Cultured
Nitrites
geography
geography.geographical_feature_category
biology
Pancreatic islets
Pancreatic Ducts
Middle Aged
Islet
Molecular biology
Immunohistochemistry
Nitric oxide synthase
Cytokine
Endocrinology
medicine.anatomical_structure
chemistry
biology.protein
Cytokines
Nitric Oxide Synthase
Subjects
Details
- ISSN :
- 00121797
- Volume :
- 48
- Issue :
- 1
- Database :
- OpenAIRE
- Journal :
- Diabetes
- Accession number :
- edsair.doi.dedup.....054d3265bc809975864822a3e5b26cf3