Biological effects of Ni(II) on monocytes and macrophages in normal and hyperglycemic environments

Monica Chana, Jill B. Lewis, Ryan Davis, Yolanda Elam, David Hobbs, Petra E. Lockwood, John C. Wataha, Regina L W Messer

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)2433-2439
Number of pages7
JournalJournal of Biomedical Materials Research - Part A
Volume106
Issue number9
DOIs
StatePublished - Sep 1 2018

Fingerprint

Macrophages
Nickel
Monocytes
Corrosion
Ions
Cytokines
Dental alloys
Dental Alloys
Toxicity
Interleukin-6
Tooth
Cells
Inflammation

Keywords

  • THP
  • hyperglycemia
  • macrophages
  • monocytes
  • nickel

ASJC Scopus subject areas

  • Ceramics and Composites
  • Biomaterials
  • Biomedical Engineering
  • Metals and Alloys

Cite this

Biological effects of Ni(II) on monocytes and macrophages in normal and hyperglycemic environments. / Chana, Monica; Lewis, Jill B.; Davis, Ryan; Elam, Yolanda; Hobbs, David; Lockwood, Petra E.; Wataha, John C.; Messer, Regina L W.

In: Journal of Biomedical Materials Research - Part A, Vol. 106, No. 9, 01.09.2018, p. 2433-2439.

Research output: Contribution to journalArticle

Chana, Monica ; Lewis, Jill B. ; Davis, Ryan ; Elam, Yolanda ; Hobbs, David ; Lockwood, Petra E. ; Wataha, John C. ; Messer, Regina L W. / Biological effects of Ni(II) on monocytes and macrophages in normal and hyperglycemic environments. In: Journal of Biomedical Materials Research - Part A. 2018 ; Vol. 106, No. 9. pp. 2433-2439.
@article{036e8a4e5a1945f382055a4429d62a8f,
title = "Biological effects of Ni(II) on monocytes and macrophages in normal and hyperglycemic environments",
abstract = "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.",
keywords = "THP, hyperglycemia, macrophages, monocytes, nickel",
author = "Monica Chana and Lewis, {Jill B.} and Ryan Davis and Yolanda Elam and David Hobbs and Lockwood, {Petra E.} and Wataha, {John C.} and Messer, {Regina L W}",
year = "2018",
month = "9",
day = "1",
doi = "10.1002/jbm.a.36437",
language = "English (US)",
volume = "106",
pages = "2433--2439",
journal = "Journal of Biomedical Materials Research - Part A",
issn = "0021-9304",
publisher = "Heterocorporation",
number = "9",

}

TY - JOUR

T1 - Biological effects of Ni(II) on monocytes and macrophages in normal and hyperglycemic environments

AU - Chana, Monica

AU - Lewis, Jill B.

AU - Davis, Ryan

AU - Elam, Yolanda

AU - Hobbs, David

AU - Lockwood, Petra E.

AU - Wataha, John C.

AU - Messer, Regina L W

PY - 2018/9/1

Y1 - 2018/9/1

N2 - 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.

AB - 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.

KW - THP

KW - hyperglycemia

KW - macrophages

KW - monocytes

KW - nickel

UR - http://www.scopus.com/inward/record.url?scp=85053912736&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85053912736&partnerID=8YFLogxK

U2 - 10.1002/jbm.a.36437

DO - 10.1002/jbm.a.36437

M3 - Article

AN - SCOPUS:85053912736

VL - 106

SP - 2433

EP - 2439

JO - Journal of Biomedical Materials Research - Part A

JF - Journal of Biomedical Materials Research - Part A

SN - 0021-9304

IS - 9

ER -