scholarly journals Assessment of intestinal macromolecular absorption in young piglets to pave the way to oral vaccination: preliminary results

2021 ◽  
Author(s):  
Brodie Deluco ◽  
Heather L. Wilson
Keyword(s):  
Small Intestine ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Immune Protection ◽  
Oral Vaccination ◽  
Recycling Endosome ◽  
Late Endosomes ◽  
Small Intestinal ◽  
The Relationship ◽  
Prior Processing

AbstractThe small intestine of the piglet has evolved to be permeable immediately after birth to facilitate the uptake of colostrum-derived immunoglobulins as well as other macromolecules, and cells. However, the precise timing of gut closure in today’s precocious pig is not known. We gavaged piglets immediately after birth and at 1-h after birth with Cy5-labeled Ovalbumin (Cy5-Ova) then harvested their small intestine’s 6–7 h later. To assess localization of Cy5-Ova in the small intestinal epithelial cells, we performed immunohistochemistry using a basolateral surface marker and a recycling endosome marker called pIgR, the late endosomal marker Rab7, and the lysosomal marker LAMP-1. Cy5-Ova co-localized with Rab7 and LAMP-1 in the duodenum and jejunum of 0-h old and 1-h old gavaged piglets, but only in the ileum of 0-h gavaged piglets. These data suggest that movement of Cy5-Ova through the late endosomes to the lysosomes was much reduced in the ileum of 1-h gavaged piglets. Cy5-Ova was largely present in epithelial cell digestive and transport vacuoles, but it did not colocalize with pIgR-positive endosomes in 0-h and 1-h gavaged piglets. Differences in macromolecular uptake across the different regions of the small intestine after only 1-h may be due to prior processing of colostral macromolecules, changes in the intestine due to initiation of colonization by microflora and/or the initiation of gut-closure. Understanding the relationship between the localization of Cy5-Ova and small intestinal permeability may contribute to establishing whether oral vaccination in the newborn can capitalize on the transient permeability before gut closure to promote immune protection.

scholarly journals Immunocytochemical localization of ornithine transcarbamylase in rat intestinal mucosa. Light and electron microscopic study.

1988 ◽  
Vol 36 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Y Hamano ◽  
H Kodama ◽  
M Yanagisawa ◽  
Y Haraguchi ◽  
M Mori ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Small Intestine ◽  
Epithelial Cells ◽  
Light Microscopy ◽  
Intestinal Mucosa ◽  
Intestinal Epithelial Cells ◽  
Protein A ◽  
Intestinal Epithelial ◽  
Electron Microscopic ◽  
Small Intestinal

We investigated light and electron microscopic localization of ornithine transcarbamylase (OTC) in rat intestinal mucosa. In the immunoblotting assay of OTC-related protein, a single protein band with a molecular weight of about 36,500 is observed in extracts of liver and small intestinal mucosa but is not observed in those of stomach and large intestine. For light microscopy, tissue slices of the digestive system were embedded in Epon and stained by using anti-bovine OTC rabbit IgG and the immunoenzyme technique. For electron microscopy, slices of these and the liver tissues were embedded in Lowicryl K4M and stained by the protein A-gold technique. By light microscopy, the absorptive epithelial cells of duodenum, jejunum, and ileum stained positively for OTC, but stomach, large intestine, rectum, and propria mucosa of small intestine were not stained. Electron microscopy showed that gold particles representing the antigenic sites for OTC were confined to the mitochondrial matrix of hepatocytes and small intestinal epithelial cells. However, the enzyme was detected in mitochondria of neither liver endothelial cells, submucosal cells of small intestine, nor large intestinal epithelial cells. Labeling density of mitochondria in the absorptive epithelial cells of duodenum, jejunum, and ileum was about half of that in liver cells.

scholarly journals Small intestine barrier function failure induces systemic inflammation in monosodium glutamate-induced chronically obese mice

2019 ◽  
Vol 44 (6) ◽  
pp. 587-594 ◽  
Author(s):  
Kazuhiko Nakadate ◽  
Tomoya Hirakawa ◽  
Sawako Tanaka-Nakadate
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Systemic Inflammation ◽  
Intestinal Epithelial Cells ◽  
Monosodium Glutamate ◽  
Intestinal Epithelial ◽  
Obese Mice ◽  
Gastrointestinal Barrier ◽  
Small Intestinal ◽  
Functional Deterioration

Chronic obesity has increased worldwide, in conjunction with type 2 diabetes. Chronic obesity causes systemic inflammation that may result in functional deterioration of the gastrointestinal barrier. However, gastrointestinal conditions associated with chronic obesity have not been comprehensively investigated. The purpose of this study was to evaluate morphological changes in small intestine barrier structures during chronic obesity. A mouse model of chronic obesity induced by monosodium glutamate treatment was established. At postnatal week 15, pathological changes including in small intestinal epithelial cells were analyzed in chronically obese mice compared with controls. Numerous gaps were identified between small intestinal epithelial cells in chronically obese mice, and levels of both desmosomal and tight junction proteins were significantly lower in their small intestinal epithelial cells. Moreover, in chronically obese mice, a significant increase in the number of intestinal inflammatory cells, particularly macrophages, was observed; in addition, blood samples from the mouse model show an increase in markers of inflammation, tumor necrosis factor-alpha and interleukin-1-beta. These findings suggest that functional deterioration of adhesion structures between small intestinal epithelial cells causes gastrointestinal barrier function failure, leading to a rise in intestinal permeability to blood vessels and consequent systemic inflammation, characterized by macrophage infiltration.

scholarly journals miRNA-30e regulates abnormal differentiation of small intestinal epithelial cells in diabetic mice by downregulating Dll4 expression

2016 ◽  
Vol 49 (1) ◽  
pp. 102-114 ◽  
Author(s):  
Ti-Dong Shan ◽  
Hui Ouyang ◽  
Tao Yu ◽  
Jie-Yao Li ◽  
Can-Ze Huang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Diabetic Mice ◽  
Small Intestinal

scholarly journals Mitochondrial gene expression in small intestinal epithelial cells

1995 ◽  
Vol 308 (2) ◽  
pp. 665-671 ◽  
Author(s):  
T P Mayall ◽  
I Bjarnason ◽  
U Y Khoo ◽  
T J Peters ◽  
A J S Macpherson
Keyword(s):  
Epithelial Cells ◽  
Cytochrome Oxidase ◽  
Cytochrome B ◽  
Intestinal Epithelial Cells ◽  
Mitochondrial Gene ◽  
Cytochrome Oxidase I ◽  
Mrna Levels ◽  
Intestinal Epithelial ◽  
Mitochondrial Transcription Factor ◽  
Small Intestinal

Most mitochondrial genes are transcribed as a single large transcript from the heavy strand of mitochondrial DNA, and are subsequently processed into the proximal mitochondrial (mt) 12 S and 16 S rRNAs, and the more distal tRNAs and mRNAs. We have shown that in intestinal epithelial biopsies the steady-state levels of mt 12 S and 16 S rRNA are an order of magnitude greater than those of mt mRNAs. Fractionation of rat small intestinal epithelial cells on the basis of their maturity has shown that the greatest ratios of 12 S mt rRNA/cytochrome b mt mRNA or 12 S mt rRNA/cytochrome oxidase I mt mRNA are found in the surface mature enterocytes, with a progressive decrease towards the crypt immature enteroblasts. Cytochrome b and cytochrome oxidase I mt mRNA levels are relatively uniform along the crypt-villus axis, but fractionation experiments showed increased levels in the crypt base. The levels of human mitochondrial transcription factor A are also greater in immature crypt enteroblasts compared with mature villus enterocytes. These results show that the relative levels of mt rRNA and mRNA are distinctly regulated in intestinal epithelial cells according to the crypt-villus position and differentiation status of the cells, and that there are higher mt mRNA and mt TFA levels in the crypts, consistent with increased transcriptional activity during mitochondrial biogenesis in the immature enteroblasts.

Effect of leptin on intestinal apolipoprotein AIV in response to lipid feeding

2001 ◽  
Vol 281 (3) ◽  
pp. R753-R759 ◽  
Author(s):  
Takashi Doi ◽  
Min Liu ◽  
Randy J. Seeley ◽  
Stephen C. Woods ◽  
Patrick Tso
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Regional Distribution ◽  
Intestinal Epithelial ◽  
Lipid Infusion ◽  
Intraduodenal Infusion ◽  
Crypt Cells

We determined apolipoprotein AIV (apo AIV) content in intestinal epithelial cells using immunohistochemistry when leptin was administered intravenously. Most of the apo AIV immunoreactivity in the untreated intestine was located in the villous cells as opposed to the crypt cells. Regional distribution of apo AIV immunostaining revealed low apo AIV content in the duodenum and high content in the jejunum that gradually decreases caudally toward the ileum. Intraduodenal infusion of lipid (4 h) significantly increased apo AIV immunoreactivity in the jejunum and ileum. Simultaneous intravenous leptin infusion plus duodenal lipid infusion markedly suppressed apo AIV immunoreactivity. Duodenal lipid infusion increased plasma apo AIV significantly (measured by ELISA), whereas simultaneous leptin infusion attenuated the increase. These findings suggest that leptin may regulate circulating apo AIV by suppressing apo AIV synthesis in the small intestine.

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