Limits...
Intestinal inflammation in rats induces metallothionein in colonic submucosa.

Al-Gindan Y, Shawarby M, Noto A, Taylor CG - J Clin Biochem Nutr (2009)

Bottom Line: Serum zinc concentrations were attenuated in the DSS-challenged ZT and ZS groups suggesting that zinc was being utilized in some capacity in response to inflammation.DSS-challenge induced MT immunostaining in the colonic submucosa, however, MT was not associated with histological improvements in the present study.The site-specific MT induction in colonic submucosa during intestinal inflammation requires further clarification as a component of the host defense.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, MB R3T 2N2, Canada.

ABSTRACT
The aim of the current study was to determine if induction of metallothionein (MT) via acute or chronic dietary zinc supplementation attenuates intestinal inflammation, and to investigate the relationship with site-specific intestinal MT determined by immunolocalization. Growing rats were assigned to zinc-deficient (ZD), acute zinc-treated (ZT), pair-fed, control or chronic Zn-supplemented (ZS) groups. Half the rats in each dietary group received 5% dextran sulphate sodium (DSS) in their drinking water for 4 days. DSS treatment produced acute intestinal inflammation in the colon only, however, dietary zinc deficiency, acute zinc treatment or chronic zinc supplementation did not alter the severity of ulceration. Serum zinc concentrations were attenuated in the DSS-challenged ZT and ZS groups suggesting that zinc was being utilized in some capacity in response to inflammation. DSS-challenge induced MT immunostaining in the colonic submucosa, however, MT was not associated with histological improvements in the present study. The site-specific MT induction in colonic submucosa during intestinal inflammation requires further clarification as a component of the host defense.

No MeSH data available.


Related in: MedlinePlus

Small intestinal metallothionein localization. Metallothionein was absent in the ZD groups (A–B) and present in all other groups (C–J) as indicated by scoring: (−−) none to very few cells, (+) mild, (++) moderate, (+++) high. PC = Paneth cells, SEC = surface epithelial cells, GC = goblet cells and LP = lamina propria. DSS– = no dextran sulfate sodium challenge, DSS+ = 5% dextran sulfate sodium challenge; ZD = zinc deficient (3 mg/kg zinc), PF = pair fed (30 mg/kg zinc) to match energy intake of ZD group, ZT = zinc deficient (3 mg/kg zinc) and repleted (300 mg/kg zinc), C = control (30 mg/kg zinc), ZS = zinc supplemented (300 mg/kg zinc). All slides 10× magnification.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2654469&req=5

Figure 4: Small intestinal metallothionein localization. Metallothionein was absent in the ZD groups (A–B) and present in all other groups (C–J) as indicated by scoring: (−−) none to very few cells, (+) mild, (++) moderate, (+++) high. PC = Paneth cells, SEC = surface epithelial cells, GC = goblet cells and LP = lamina propria. DSS– = no dextran sulfate sodium challenge, DSS+ = 5% dextran sulfate sodium challenge; ZD = zinc deficient (3 mg/kg zinc), PF = pair fed (30 mg/kg zinc) to match energy intake of ZD group, ZT = zinc deficient (3 mg/kg zinc) and repleted (300 mg/kg zinc), C = control (30 mg/kg zinc), ZS = zinc supplemented (300 mg/kg zinc). All slides 10× magnification.

Mentions: Moderate to strong cytoplasmic and nuclear MT staining of Paneth cells (PC), surface epithelial cells (SEC), goblet cells (GC) and lamina propria (LP) was present in all groups with the exception of the ZD group which had no to very weak (one to two cells only) MT staining (Fig. 4A, B). The strongest and the most consistent MT immunostaining of Paneth cells, surface epithelial cells, goblet cells and lamina propria was seen in the unchallenged ZS rats (Fig. 4J). There was strong MT immunostaining in Paneth cells and moderate immunostaining in surface epithelial cells, goblet cells and lamina propria in all other groups except the ZD rats which had very weak to no detectable MT immunostaining (Fig. 4).


Intestinal inflammation in rats induces metallothionein in colonic submucosa.

Al-Gindan Y, Shawarby M, Noto A, Taylor CG - J Clin Biochem Nutr (2009)

Small intestinal metallothionein localization. Metallothionein was absent in the ZD groups (A–B) and present in all other groups (C–J) as indicated by scoring: (−−) none to very few cells, (+) mild, (++) moderate, (+++) high. PC = Paneth cells, SEC = surface epithelial cells, GC = goblet cells and LP = lamina propria. DSS– = no dextran sulfate sodium challenge, DSS+ = 5% dextran sulfate sodium challenge; ZD = zinc deficient (3 mg/kg zinc), PF = pair fed (30 mg/kg zinc) to match energy intake of ZD group, ZT = zinc deficient (3 mg/kg zinc) and repleted (300 mg/kg zinc), C = control (30 mg/kg zinc), ZS = zinc supplemented (300 mg/kg zinc). All slides 10× magnification.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2654469&req=5

Figure 4: Small intestinal metallothionein localization. Metallothionein was absent in the ZD groups (A–B) and present in all other groups (C–J) as indicated by scoring: (−−) none to very few cells, (+) mild, (++) moderate, (+++) high. PC = Paneth cells, SEC = surface epithelial cells, GC = goblet cells and LP = lamina propria. DSS– = no dextran sulfate sodium challenge, DSS+ = 5% dextran sulfate sodium challenge; ZD = zinc deficient (3 mg/kg zinc), PF = pair fed (30 mg/kg zinc) to match energy intake of ZD group, ZT = zinc deficient (3 mg/kg zinc) and repleted (300 mg/kg zinc), C = control (30 mg/kg zinc), ZS = zinc supplemented (300 mg/kg zinc). All slides 10× magnification.
Mentions: Moderate to strong cytoplasmic and nuclear MT staining of Paneth cells (PC), surface epithelial cells (SEC), goblet cells (GC) and lamina propria (LP) was present in all groups with the exception of the ZD group which had no to very weak (one to two cells only) MT staining (Fig. 4A, B). The strongest and the most consistent MT immunostaining of Paneth cells, surface epithelial cells, goblet cells and lamina propria was seen in the unchallenged ZS rats (Fig. 4J). There was strong MT immunostaining in Paneth cells and moderate immunostaining in surface epithelial cells, goblet cells and lamina propria in all other groups except the ZD rats which had very weak to no detectable MT immunostaining (Fig. 4).

Bottom Line: Serum zinc concentrations were attenuated in the DSS-challenged ZT and ZS groups suggesting that zinc was being utilized in some capacity in response to inflammation.DSS-challenge induced MT immunostaining in the colonic submucosa, however, MT was not associated with histological improvements in the present study.The site-specific MT induction in colonic submucosa during intestinal inflammation requires further clarification as a component of the host defense.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, MB R3T 2N2, Canada.

ABSTRACT
The aim of the current study was to determine if induction of metallothionein (MT) via acute or chronic dietary zinc supplementation attenuates intestinal inflammation, and to investigate the relationship with site-specific intestinal MT determined by immunolocalization. Growing rats were assigned to zinc-deficient (ZD), acute zinc-treated (ZT), pair-fed, control or chronic Zn-supplemented (ZS) groups. Half the rats in each dietary group received 5% dextran sulphate sodium (DSS) in their drinking water for 4 days. DSS treatment produced acute intestinal inflammation in the colon only, however, dietary zinc deficiency, acute zinc treatment or chronic zinc supplementation did not alter the severity of ulceration. Serum zinc concentrations were attenuated in the DSS-challenged ZT and ZS groups suggesting that zinc was being utilized in some capacity in response to inflammation. DSS-challenge induced MT immunostaining in the colonic submucosa, however, MT was not associated with histological improvements in the present study. The site-specific MT induction in colonic submucosa during intestinal inflammation requires further clarification as a component of the host defense.

No MeSH data available.


Related in: MedlinePlus