Biological effects of Ni(II) on monocytes and macrophages in normal and hyperglycemic environments
| Autor: | Monica Chana, Petra E. Lockwood, Jill Lewis, Yolanda Elam, David T. Hobbs, John C. Wataha, Regina L. W. Messer, Ryan R. Davis |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Materials science Dental alloys Metals and Alloys Biomedical Engineering Inflammation Context (language use) Monocyte proliferation Biomaterials 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Endocrinology Internal medicine Toxicity Ceramics and Composites medicine Nickel ions Cytokine secretion Secretion medicine.symptom 030217 neurology & neurosurgery |
| Zdroj: | Journal of Biomedical Materials Research Part A. 106:2433-2439 |
| ISSN: | 1549-3296 |
| Popis: | Corrosion and release of nickel ions from biomedical alloys are well documented, but little is still known about the effects of released nickel ions on cellular function with recurrent inflammatory challenges. Evidence suggests Ni(II) ions amplify LPS-induced secretion of several pro-inflammatory cytokines from monocytes. Exacerbating the inflammatory response, hyperglycemic conditions also affect monocytic function. This study investigated how Ni(II) and hyperglycemic conditions, both singly and in combination, alter monocyte proliferation, mitochondrial activity, inflammatory responses, and differentiation. Results showed that Ni(II) did not affect proliferation, but decreased mitochondrial activity in monocytic-cells and macrophages under normal conditions. However, hyperglycemic conditions negated the toxicity seen with Ni(II) exposure. Cytokine secretion in response to LPS was variable, with little effect on IL6 secretion, but significantly increased secretion of IL1β at intermediate Ni(II) concentrations. Hyperglycemic conditions did not alter these results significantly. Finally, exposure to eluants from nickel-based commercial alloys caused enhanced IL1β secretion from PMA-treated cells. These data suggest that corrosion products from nickel-containing dental alloys increased Ni(II)-induced changes in cytokine secretion by monocytes and macrophages. By better defining the effects of Ni(II) at these lower, biomedically relevant concentrations, we improve understanding of the biomedical alloy risk in the context of dental inflammation. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A:2433-2439, 2018. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text