Acesulfame‐K induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa

2021 ◽  
Author(s):  
Yoshinori Hanawa ◽  
Masaaki Higashiyama ◽  
Chie Kurihara ◽  
Rina Tanemoto ◽  
Suguru Ito ◽  
...  
Keyword(s):  
Intestinal Mucosa ◽  
Intestinal Injury ◽  
Lymphocyte Migration

scholarly journals Flaxseed, olive and fish oil influence plasmatic lipids, lymphocyte migration and morphometry of the intestinal of Wistar rats

2010 ◽  
Vol 25 (3) ◽  
pp. 275-280 ◽  
Author(s):  
Damiana Diniz Rosa ◽  
Regiane Lopes de Sales ◽  
Luis Fernando de Sousa Moraes ◽  
Fabíola Cesário Lourenço ◽  
Clóvis Andrade Neves ◽  
...  
Keyword(s):  
Fish Oil ◽  
Intestinal Mucosa ◽  
Wistar Rats ◽  
Density Lipoprotein ◽  
Parameter Analysis ◽  
Male Rats ◽  
Histological Evaluation ◽  
Control Group ◽  
Soy Oil ◽  
Lymphocyte Migration

PURPOSE: Evaluate the effect of flaxseed, olive and fish oil on the lipid profile, preservation of villosities and lymphocyte migration in the intestinal mucosa of Wistar rats. METHODS: Thirty Wistar male rats were divided into four groups, which received the AIN-93M diet, with changes only to their lipid source: flaxseed, olive, fish, and soy oil (control group). The serum was separated for the biochemical parameter analysis. A histological evaluation was performed in the ileal portion. RESULTS: The group which was fed fish oil presented lower values when compared to the other treatments for Total Cholesterol, High-density Lipoprotein Cholesterol and Triacylglycerol (p<0.05). The animals treated with fish and olive oils presented better intestinal villosities preservation. Less deposition of lymphocytes was observed in the flaxseed group (p<0.001). CONCLUSIONS: This study demonstrated that flaxseed, olive and fish oils present different responses than soy oil for the intestinal mucosa preservation and lymphocyte proliferation in Wistar rats.

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1

2004 ◽  
Vol 286 (5) ◽  
pp. G702-G710 ◽  
Author(s):  
Toshiko Ogawa ◽  
Soichiro Miura ◽  
Yoshikazu Tsuzuki ◽  
Takashi Ogino ◽  
Ken Teramoto ◽  
...  
Keyword(s):  
Food Allergy ◽  
T Lymphocytes ◽  
Intestinal Mucosa ◽  
Morphological Changes ◽  
Peyer's Patches ◽  
Brown Norway ◽  
Peyer’S Patches ◽  
Small Intestinal Mucosa ◽  
Lymphocyte Migration ◽  
Small Intestinal

Few models have described a chronic food allergy with morphological changes in the intestinal mucosa. Here we established an ovalbumin (OVA)-induced, cell-mediated, allergic rat model and examined lymphocyte migration in the gut. Brown Norway rats were intraperitoneally sensitized to OVA and then given 10 mg OVA/day by gastric intubation for 6 wk. Lymphocyte subsets and adhesion molecules were examined immunohistochemically, and the migration of T lymphocytes to microvessels of Peyer's patches and villus mucosa was observed by using an intravital microscope. Serum OVA-specific IgG and IgE levels were increased in animals repeatedly exposed to OVA. Significant villus atrophy and increased crypt depth was accompanied by increased infiltration of T lymphocytes in the small intestinal mucosa of the group given OVA. Expression of rat mast cell protease II and of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was also increased in these groups. The administration of anti-MAdCAM-1 antibody significantly attenuated the OVA-induced changes in the mucosal architecture and in CD4 T lymphocyte infiltration. Intravital observation demonstrated that in rats with a chronic allergy, T lymphocytes significantly accumulated in villus microvessels as well as in Peyer's patches via a MAdCAM-1-dependent process. Our model of chronic food allergy revealed that lymphocyte migration was increased with MAdCAM-1 upregulation.

scholarly journals In vivo demonstration of T lymphocyte migration and amelioration of ileitis in intestinal mucosa of SAMP1/Yit mice by the inhibition of MAdCAM-1

2005 ◽  
Vol 140 (1) ◽  
pp. 22-31 ◽  
Author(s):  
K. Matsuzaki ◽  
Y. Tsuzuki ◽  
H. Matsunaga ◽  
T. Inoue ◽  
J. Miyazaki ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Intestinal Mucosa ◽  
Lymphocyte Migration

scholarly journals Gene expression analysis in NSAID-induced rat small intestinal disease model with the intervention of berberine by the liquid chip technology

2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Guanqun Chao ◽  
Qianqian Wang ◽  
Fangxu Ye ◽  
Shuo Zhang
Keyword(s):  
Intestinal Mucosa ◽  
Intervention Group ◽  
Tube Feeding ◽  
Intestinal Injury ◽  
Control Group ◽  
Model Group ◽  
Chip Technology ◽  
Small Intestinal Injury ◽  
Small Intestinal ◽  
Histology Score

Abstract Objective Investigate the effect and mechanism of berberine on the small intestinal mucosa of non-steroidal anti-inflammatory drugs (NSAIDs) related small intestinal injury. Materials and methods Twenty-four SD rats were randomly divided into control group, model group and intervention group. The model group and intervention group were treated with diclofenac (7.5 mg/kg·d, 2/d), a total of 4 days tube feeding, and the intervention group was treated with 50 mg/kg·d intragastric administration of berberine after 2 days. The control group was treated with 7.5 mg/kg·d, 2/d 0.9% saline tube feeding. Then we screened differential expression of colonic mucosal gene by the liquid chip technology. Results Compared with the control group, macroscopic and histology score of the model group increased significantly (P < 0.05), HTR4, HTR1a, F2RL3, CALCA, NPY, CRHR2, IL1b, P2RX3, TPH1, HMOX1, TRPV1, VIP, F2RL1, SLC6A4, TFF2, AQP8 content were significantly increased (P < 0.05), NOS1 content decreased significantly (P < 0.05); Compared with the model group, macroscopic and histology score of the intervention group improved significantly (P < 0.05), and HTR4, F2RL3, NPY, CRHR2, IL1b, VIP, AQP8 content were significantly lower (P < 0.05), NOS1 content increased significantly (P < 0.05). Conclusion Berberine has a protective effect on NSAID-associated small intestinal injury, the mechanism may be that berberine decreases the expression of intestinal mucosa HTR4, F2RL3, NPY, CRHR2, IL1b, VIP, AQP8, and increases the expression of NOS1, that to reduce intestinal permeability and protect intestinal mucosal barrier.

scholarly journals Asparagine attenuates intestinal injury, improves energy status and inhibits AMP-activated protein kinase signalling pathways in weaned piglets challenged with Escherichia coli lipopolysaccharide

2015 ◽  
Vol 114 (4) ◽  
pp. 553-565 ◽  
Author(s):  
Xiuying Wang ◽  
Yulan Liu ◽  
Shuang Li ◽  
Dingan Pi ◽  
Huiling Zhu ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Intestinal Mucosa ◽  
Tricarboxylic Acid Cycle ◽  
Intestinal Injury ◽  
Intestinal Morphology ◽  
Intestinal Damage ◽  
Adenylate Energy Charge ◽  
Energy Status ◽  
Weaned Piglets ◽  
Amp Activated Protein Kinase

The intestine requires a high amount of energy to maintain its health and function; thus, energy deficits in intestinal mucosa may lead to intestinal damage. Asparagine (Asn) is a precursor for many other amino acids such as aspartate, glutamine and glutamate, which can be used to supply energy to enterocytes. In the present study, we hypothesise that dietary supplementation of Asn could alleviate bacterial lipopolysaccharide (LPS)-induced intestinal injury via improvement of intestinal energy status. A total of twenty-four weaned piglets were assigned to one of four treatments: (1) non-challenged control; (2) LPS+0 % Asn; (3) LPS+0·5 % Asn; (4) LPS+1·0 % Asn. On day 19, piglets were injected with LPS or saline. At 24 h post-injection, piglets were slaughtered and intestinal samples were collected. Asn supplementation improved intestinal morphology, indicated by higher villus height and villus height:crypt depth ratio, and lower crypt depth. Asn supplementation also increased the ratios of RNA:DNA and protein:DNA as well as disaccharidase activities in intestinal mucosa. In addition, Asn supplementation attenuated bacterial LPS-induced intestinal energy deficits, indicated by increased ATP and adenylate energy charge levels, and decreased AMP:ATP ratio. Moreover, Asn administration increased the activities of key enzymes involved in the tricarboxylic acid cycle, including citrate synthase, isocitrate dehydrogenase and α-ketoglutarate dehydrogenase complex. Finally, Asn administration decreased the mRNA abundance of intestinal AMP-activated protein kinase-α1 (AMPKα1), AMPKα2, silent information regulator 1 (SIRT1) and PPARγ coactivator-1α (PGC1α), and reduced intestinal AMPKα phosphorylation. Collectively, these results indicate that Asn supplementation alleviates bacterial LPS-induced intestinal injury by modulating the AMPK signalling pathway and improving energy status.

scholarly journals INCREASED TRAFFICKING OF MESENTERIC LYMPH-DERIVED γδ T CELLS INTO INTESTINAL MUCOSA IS ASSOCIATED WITH GUT INJURY AFTER INTESTINAL ISCHEMIA-REPERFUSION IN RATS

Lymphology ◽  
2019 ◽  
Vol 52 (2) ◽  
Author(s):  
J Yang ◽  
Y Shen ◽  
RQ Wu ◽  
H Zhu ◽  
Y Jin ◽  
...  
Keyword(s):  
T Cells ◽  
Intestinal Mucosa ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Γδ T Cells ◽  
Intestinal Injury ◽  
Endotoxin Concentration ◽  
Mesenteric Lymph ◽  
Tnf Α ◽  
Intestinal Ischemia Reperfusion

We sought to investigate the effects of mesenteric lymph-derived γδ T cells trafficking into intestinal mucosa on gut injury after intestinal ischemia-reperfusion (IIR). γδ T cells were separated from mesenteric lymph and then infused into the femoral vein of rats after the γδ T cells were labeled with 51Cr. Migration of γδ T cells in vivo across the intestinal mucosa was determined by γ-counter. Meanwhile, TNF-α activity and endotoxin concentration in mesenteric lymph were detected. The population of γδ T cells of Peyer's patches in the small intestines was analyzed by immunofluorescence double staining methods and flow cytometry. After IIR injury, the mean optical density value (MOD) and population of γδ T cells in Peyer's patches of the gut and migration of 51Cr-γδ T cells across the intestinal mucosa were significantly increased, which had highly positive correlations to degree of intestinal injury, TNF-α levels and endotoxin concentration in mesenteric lymph after reperfusion. The increased population of γδ T cells derived from mesenteric lymph trafficking into the intestinal mucosa might promote the small intestinal injury after IIR.

Activation of isolated heterophils from chicks stimulated in vivo with salmonella enteritidis-immune lymphokines

1996 ◽  
Vol 54 ◽  
pp. 760-761
Author(s):  
R. B. Moyes ◽  
R. E. Droleskey ◽  
M. H. Kogut ◽  
J. R. DeLoach
Keyword(s):  
Lamina Propria ◽  
Intestinal Mucosa ◽  
Salmonella Enteritidis ◽  
Intestinal Tract ◽  
Polymorphonuclear Cells ◽  
Subclinical Infection ◽  
Egg Products ◽  
Immune Lymphokines ◽  
Organ Invasion

Salmonella enteritidis (SE) is of great concern to the poultry industry due to the organism's ability to penetrate the intestinal mucosa of the laying hen and subsequently colonize the ovaries and yolk membrane. The resultant subclinical infection can lead to SE infection of raw eggs and egg products. Interference with the ability of the organism to invade has been linked to the activation and recruitment of inflammatory polymorphonuclear cells, heterophils, to the lamina propria of the intestinal tract.Recently it has been established that heterophil activation and increased resistance to SE organ invasion can be accomplished by the administration of SE-immune lymphokines (SE-ILK) obtained from supernatants of concanavalin-A stimulated SE immune T lymphocytes from SE hyperimmunized hens. Invasion of SE into the lamina propria provides a secondary signal for directing activated heterophils to the site of SE invasion.

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