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PubMed1996

Comparative alterations in p53 expression and apoptosis in the irradiated rat small and large intestine.

Temporal and spatial relationships between radiation-induced apoptosis and expression of p53 mRNA and protein were compared in rat small and large intestine. Apoptosis was quantified using morphological criteria, and p53 expression determined by immunohistochemistry or whole-tissue Northern analysis. In the small intestine, peak levels of apoptosis appeared earlier (4 h) than in the large intestine (6 h). p53 mRNA transcript levels in small and large intestine were not significantly altered from control levels at any time after treatment. However, in treated small and large intestine, cells showed increased positivity for p53 protein, increasing 10-fold over control levels 4-5 h after irradiation. A strong spatial relationship was found between high incidence apoptosis and p53 protein positivity. We compared published data of stem cell population positions for small and large intestine with our results. Target cells for apoptosis and p53 expression occurred at approximately fifth position from the crypt base of the small intestine, a zone coincident with stem cell population. Target cell position for apoptosis and p53 expression in the large intestine was again at fifth or sixth position from the base, but this zone is not the reported stem cell position (first or second position) for large intestine. Results from our model of radiation-induced intestinal apoptosis indicate that p53 protein is closely associated both temporally and spatially with the induction of apoptosis, and support the work of others in suggesting that p53 expression is modulated post-transcriptionally. Furthermore, our results support a hypothesis that apoptotic targeting of damaged stem cell populations, early response for apoptotic removal of DNA-damaged cells and/or early repair of these damage cells are all important parameters that determine differences in levels of tumorigenesis in the small and large intestine.

Animals↗
PubMed2003

Morphological properties of zero-stress state in rat large intestine during systemic EGF treatment.

Systemic treatment with epidermal growth factor (EGF) induce growth of the large intestine. The aim of this study was to investigate the morphological properties early in the course of EGF-induced large intestinal growth. The effects of systemic EGF treatment on the morphological properties at the zero-stress state along the large intestine were investigated. EGF-treated rats and control rats were allocated into group with EGF treatment for 2, 4, 7, and 14 days (N = 6 for each EGF treatment group except N = 4 for the 14-day group). The controls had saline injected (N = 3 for each group). The excised large intestine was subdivided into four segments: the ascending colon, transverse colon, descending colon, and rectum. The length and weight of each segment was measured. The zero-stress state was obtained by cutting rings of the large intestine radially, and the opening angle was measued on video images. The thickness and cross-sectional area of the mucosa and muscle layers, and the inner and outer circumference were measured. The total colon length did not increase, whereas the weight of the large intestine, muscosal thickness and mass, and inner and outer circumference increased significantly (P < 0.05). The increase was most prominent in the proximal colon after 7 days of EGF treatment. Later no further morphological changes were observed, except for a decrease in mucosal thickness in most segments and in mucosal cross-sectional area in the descending colon. In the controls and during the first week of EGF treatment, the opening angle was approximately 100 degrees. After 14 days the opening angle increased significantly in the ascending and transverse colon to approximately 172 and 135 degrees (P < 0.05). In conclusion, this study demonstrates that systemic EGF treatment caused remodeling of the morphology of the zero-stress state in the large intestine in a time-dependent manner. The growth was most pronounced in the ascending and transverse colon and involved mainly the mucosal layer.

Analysis of Variance↗
PubMed1989

Nutrient digestion in the large intestine as influenced by forage to concentrate ratio and forage physical form.

Digestion in the large intestine was investigated in four growing steers fitted with duodenal and ileal cannulas. Diets assigned within a 4 x 4 Latin square were: 20% long alfalfa hay and 80% grain; 15% pelleted alfalfa, 5% hay, and 80% grain; 80% hay and 20% grain; and 60% pellets, 20% hay, and 20% grain. Intake of DM was not affected by diet. Organic matter digestion in the large intestine averaged 9, 3, 1, and -4% of total tract digestion for the 20% hay, 20% pellet, 80% hay, and 80% pellet diets, respectively, with significant increases due to high grain diets and long hay. Digestion of CP in the large intestine as a percentage of total tract digestion was unaffected by diet but averaged 3, -1, .3, and -6% for the respective diets. Percentage of total tract starch digestion occurring in the large intestine increased with grain feeding and averaged 6, 3, 1, and 1%, respectively. Digestion of ADF and NDF in the large intestine as a percentage of total tract was unaffected by diet; however, the respective means were 16 and 15, 7 and 7, 5 and 15, and 1 and 1%. In a second trail the same animals were fed a more typical dairy cow diet consisting of 50% grain, 25% corn silage, and 25% long alfalfa hay for a single 18-d period. Digestion in the large intestine accounted for 2.1, .2, 3.6, and 6.4% of total tract digestion of organic matter, starch, ADF, and NDF, respectively; however, feed intake was not as great as in the first trail. Although conditions of these studies differed from those commonly experienced by lactating cows, the underlying principals should apply. The large intestine would be expected to make an even greater contribution to total tract digestion in lactating cows consuming proportionally more DM.

Animal Feed↗
PubMed2005

Activation of CD1d-independent NK1.1+ T cells in the large intestine by Lactobacilli.

Among digestive organs, the liver and the large intestine are abundant in T cells expressing NK1.1. NK1.1+ T cells in the liver are mostly CD1d-dependent whereas those in the large intestine are CD1d-independent. In this study, we investigated the effects of Lactobacilli on NK1.1+ T cells in the digestive organs of mice. C57BL/6 mice were orally given a dietary supplement prepared from mixed cultures of eight strains of Lactobacilli. Oral administration of Lactobacilli to mice resulted in the selective expansion of NK1.1+ T cells in the large intestine. These colon NK1.1+ T cells activated by Lactobacilli were found to express IFN-gamma mRNA. The level of IFN-gamma in the serum was also elevated by the administration of Lactobacilli. Our results suggest that Lactobacilli selectively activate CD1d-independent NK1.1+ T cells in the large intestine to produce IFN-gamma and therefore modulate Th1 immune responses.

Animals↗
PubMed1984

Microvilli- and desmosome-associated bodies in Crohn's disease and other disorders in childhood: an ultrastructural abnormality of the small and large intestine.

Ultrastructural studies of the small and large intestine from children revealed five cases showing abnormal small electron-dense bodies within enterocytes and goblet cells. The characteristic features of the bodies were: (a) they occurred within microvilli and within the apical part of the cell cytoplasm; (b) they showed an association with the most apically located desmosomes of the epithelial cells; (c) in the microvilli they were present within protrusions of the membrane, suggesting that they may bud out of the cell; and (d) they were not membrane-bound within the cell but were found outside the cell as luminal, membrane-bound particles. These bodies occurred in two children with Crohn's disease and in three children having other gastrointestinal disorders. Similar electron-dense bodies which did not have all of the characteristics listed above were found in a sixth child who had Crohn's disease. These electron-dense bodies do not resemble any known inclusion of intestinal epithelium, nor do they resemble any previously described microorganism, although their apparent release from the cell by a process of budding is suggestive of a microbial identity. The occurrence of these bodies in childhood Crohn's disease suggests that they may be disease-related, but their precise nature and relevance to this or other gastrointestinal disorders remain unknown.

Adolescent↗
PubMed1997

The number of clonogenic cells in crypts in three regions of murine large intestine.

Data are presented for the kinetics of repair of sub-lethal damage in the large intestine of mice. The results are based on experiments using the crypt microcolony assay with two equal sized doses which were delivered with a variable interval of time between the doses. These show that this split-dose repair was largely complete after 5 h, and that there were no significant differences between three regions of the large intestine. Overall the half-time for the repair was 2.3 +/- 0.8 h, and the maximum split-dose repair ratio (the proportion of damage recovered by splitting the dose into two fractions) was 22 +/- 2% and the mean recovery factor (the ratio of the number of surviving crypts using long interfraction intervals to that at zero time) was 11 +/- 2. The split-dose approach (Hendry 1979) using a 5 h interval has been used to estimate the number of clonogenic cells in large intestinal crypts. A range of single and paired doses between 7 Gy and 10.5 Gy were used. There were significant differences between the three regions of the large intestine, the caecum, mid-colon and rectum. The estimate of the number of clonogens also depended in a significant way on the dose of radiation used to make the estimate. At low doses large intestinal crypts contain between 5 and 10 clonogenic cells while if high doses were used they contain an estimated 16 to 36 clonogenic cells. Considerable similarity exists between the small intestine and the large intestine for; (a) the repair kinetics (b), the clonogenic estimates, and (c) their dependence on dose.

Animals↗