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Implications of compromised zinc status on bone loss associated with chronic inflammation in C57BL/6 mice.

Chongwatpol P, Rendina-Ruedy E, Stoecker BJ, Clarke SL, Lucas EA, Smith BJ - J Inflamm Res (2015)

Bottom Line: On the 6th week, mice had a slow release pellet implanted to induce a low-grade inflammation for the final 4 weeks of the study. -Zn induced a decrease in total white cell counts and peripheral lymphocytes, whereas LPS increased blood monocytes.LPS significantly reduced spine bone mineral density and trabecular bone volume and number of the vertebral body compared with both zinc adequate and inadequate without LPS groups.LPS induced an increase in TNF-α and this response was further increased with -Zn.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutritional Sciences, Oklahoma State University, Stillwater, OK, USA.

ABSTRACT
Compromised zinc status and chronic inflammation are independent factors that can contribute to bone loss. However, zinc's role in regulating lymphoid and myeloid cell populations, combined with the interplay between the immune and skeletal systems raises the question as to the extent to which a low-grade inflammatory challenge in the context of marginal zinc deficiency would exacerbate bone loss. To address this question, young adult C57BL/6 male mice (n=32) were used in a 2×2 factorial design with dietary zinc (adequate or 35 ppm vs inadequate or -Zn =5 ppm) and lipopolysaccharide (LPS, 0 or 0.1 mg/kg body weight). Mice were fed their respective diets for 10 weeks. On the 6th week, mice had a slow release pellet implanted to induce a low-grade inflammation for the final 4 weeks of the study. -Zn induced a decrease in total white cell counts and peripheral lymphocytes, whereas LPS increased blood monocytes. LPS significantly reduced spine bone mineral density and trabecular bone volume and number of the vertebral body compared with both zinc adequate and inadequate without LPS groups. Likewise, the most pronounced effects on bone strength occurred with LPS, however, -Zn also had negative effects on the bone von Mises stresses. LPS induced an increase in TNF-α and this response was further increased with -Zn. Although the marginal zinc deficiency altered immune function, bone loss was not exacerbated with low-grade chronic inflammation in marginally zinc-deficient young adult mice. These findings demonstrate that in young adult animals an immune challenge modestly increases the inflammatory response and worsens bone biomechanics in the context of a marginal zinc deficiency, but not to the extent that more severe adverse outcomes are observed on bone structural parameters.

No MeSH data available.


Related in: MedlinePlus

Comparison of hepatic tumor necrosis factor-α (TNF-α) protein levels of mice consuming zinc adequate (Con) or inadequate (−Zn) diet with (1 mg/kg body weight) or without (0 mg/kg body weight) lipopolysaccharide (LPS) treatment. Bars with # indicate an LPS main effect (P<0.05). Bars that share the same superscript letters are not significantly different from each other (Diet × LPS; P<0.05).
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f3-jir-8-117: Comparison of hepatic tumor necrosis factor-α (TNF-α) protein levels of mice consuming zinc adequate (Con) or inadequate (−Zn) diet with (1 mg/kg body weight) or without (0 mg/kg body weight) lipopolysaccharide (LPS) treatment. Bars with # indicate an LPS main effect (P<0.05). Bars that share the same superscript letters are not significantly different from each other (Diet × LPS; P<0.05).

Mentions: As anticipated, hepatic TNF-α protein was elevated in response to LPS. Although zinc deficiency has been shown to increase pro-inflammatory cytokine production, the marginal zinc deficiency alone that was achieved in this study did not alter TNF-α protein in the liver. However, TNF-α in the −Zn/+LPS group was significantly higher than the Con/−LPS (∼25%) and Con/+LPS groups (∼19%) and tended to be elevated (P=0.072) in the −Zn/−LPS group (Figure 3).


Implications of compromised zinc status on bone loss associated with chronic inflammation in C57BL/6 mice.

Chongwatpol P, Rendina-Ruedy E, Stoecker BJ, Clarke SL, Lucas EA, Smith BJ - J Inflamm Res (2015)

Comparison of hepatic tumor necrosis factor-α (TNF-α) protein levels of mice consuming zinc adequate (Con) or inadequate (−Zn) diet with (1 mg/kg body weight) or without (0 mg/kg body weight) lipopolysaccharide (LPS) treatment. Bars with # indicate an LPS main effect (P<0.05). Bars that share the same superscript letters are not significantly different from each other (Diet × LPS; P<0.05).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4508086&req=5

f3-jir-8-117: Comparison of hepatic tumor necrosis factor-α (TNF-α) protein levels of mice consuming zinc adequate (Con) or inadequate (−Zn) diet with (1 mg/kg body weight) or without (0 mg/kg body weight) lipopolysaccharide (LPS) treatment. Bars with # indicate an LPS main effect (P<0.05). Bars that share the same superscript letters are not significantly different from each other (Diet × LPS; P<0.05).
Mentions: As anticipated, hepatic TNF-α protein was elevated in response to LPS. Although zinc deficiency has been shown to increase pro-inflammatory cytokine production, the marginal zinc deficiency alone that was achieved in this study did not alter TNF-α protein in the liver. However, TNF-α in the −Zn/+LPS group was significantly higher than the Con/−LPS (∼25%) and Con/+LPS groups (∼19%) and tended to be elevated (P=0.072) in the −Zn/−LPS group (Figure 3).

Bottom Line: On the 6th week, mice had a slow release pellet implanted to induce a low-grade inflammation for the final 4 weeks of the study. -Zn induced a decrease in total white cell counts and peripheral lymphocytes, whereas LPS increased blood monocytes.LPS significantly reduced spine bone mineral density and trabecular bone volume and number of the vertebral body compared with both zinc adequate and inadequate without LPS groups.LPS induced an increase in TNF-α and this response was further increased with -Zn.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutritional Sciences, Oklahoma State University, Stillwater, OK, USA.

ABSTRACT
Compromised zinc status and chronic inflammation are independent factors that can contribute to bone loss. However, zinc's role in regulating lymphoid and myeloid cell populations, combined with the interplay between the immune and skeletal systems raises the question as to the extent to which a low-grade inflammatory challenge in the context of marginal zinc deficiency would exacerbate bone loss. To address this question, young adult C57BL/6 male mice (n=32) were used in a 2×2 factorial design with dietary zinc (adequate or 35 ppm vs inadequate or -Zn =5 ppm) and lipopolysaccharide (LPS, 0 or 0.1 mg/kg body weight). Mice were fed their respective diets for 10 weeks. On the 6th week, mice had a slow release pellet implanted to induce a low-grade inflammation for the final 4 weeks of the study. -Zn induced a decrease in total white cell counts and peripheral lymphocytes, whereas LPS increased blood monocytes. LPS significantly reduced spine bone mineral density and trabecular bone volume and number of the vertebral body compared with both zinc adequate and inadequate without LPS groups. Likewise, the most pronounced effects on bone strength occurred with LPS, however, -Zn also had negative effects on the bone von Mises stresses. LPS induced an increase in TNF-α and this response was further increased with -Zn. Although the marginal zinc deficiency altered immune function, bone loss was not exacerbated with low-grade chronic inflammation in marginally zinc-deficient young adult mice. These findings demonstrate that in young adult animals an immune challenge modestly increases the inflammatory response and worsens bone biomechanics in the context of a marginal zinc deficiency, but not to the extent that more severe adverse outcomes are observed on bone structural parameters.

No MeSH data available.


Related in: MedlinePlus