scholarly journals Metabolomic Analysis of the Liver of a Dextran Sodium Sulfate-Induced Acute Colitis Mouse Model: Implications of the Gut–Liver Connection

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 341 ◽  
Author(s):  
Sou Hyun Kim ◽  
Wonho Lee ◽  
Doyoung Kwon ◽  
Seunghyun Lee ◽  
Seung Won Son ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Sodium Sulfate ◽  
Intestinal Inflammation ◽  
Liver Metabolism ◽  
Dextran Sodium Sulfate ◽  
Proton Nuclear Magnetic Resonance ◽  
Resonance Spectroscopy ◽  
Nucleotide Synthesis ◽  
Orthogonal Projections ◽  
Latent Structures

The incidence of ulcerative colitis (UC) is increasing worldwide, and it has become a growing problem in Asia. Previous research on UC has focused on serum, plasma, urine, gut tissues, and fecal metabolic profiling, but a comprehensive investigation into the correlation between the severity of colitis and changes in liver metabolism is still lacking. Since the liver and gut exchange nutrients and metabolites through a complex network, intestinal diseases can affect both the liver and other organs. In the present study, concentration-dependent dextran sodium sulfate (DSS)-induced ulcerative colitis was employed to examine changes in liver metabolism using a proton nuclear magnetic resonance spectroscopy (1H-NMR)-and ultra-performance liquid chromatography time of flight mass spectroscopy (UPLC-TOF MS)-based metabolomics study. Using the multivariate statistical analysis method orthogonal projections to latent structures discriminant analysis (OPLS-DA), changes in metabolites depending on the DSS dose could be clearly distinguished. Specifically, hepatic metabolites involved in one-carbon metabolism, carnitine-related metabolism, and nucleotide synthesis were found to be affected by intestinal inflammation, implying the existence of a metabolic connection between the gut and liver. We are currently investigating the significance of this metabolic condition in UC.

scholarly journals Interleukin-10 is Differentially Expressed in the Small Intestine and the Colon Experiencing Chronic Inflammation and Ulcerative Colitis Induced by Dextran Sodium Sulfate in Young Pigs

2017 ◽  
pp. 147-162 ◽  
Author(s):  
D. LACKEYRAM ◽  
D. YOUNG ◽  
C. J. KIM ◽  
C. YANG ◽  
T. L. ARCHBOLD ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Chronic Inflammation ◽  
Chronic Ulcerative Colitis ◽  
Sodium Sulfate ◽  
Intestinal Inflammation ◽  
Interleukin 10 ◽  
Dextran Sodium Sulfate ◽  
Mrna Abundance ◽  
Control Group ◽  
Young Pigs

Intestinal inflammation induced with dextran sodium sulfate (DSS) is used to study acute or chronic ulcerative colitis in animal models. Decreased gut tissue anti-inflammatory cytokine IL-10 concentration and mRNA abundance are associated with the development of chronic bowel inflammation. Twelve piglets of 3 days old were fitted with an intragastric catheter and randomly allocated into control and DSS groups by administrating either sterile saline or 1.25 g of DSS/kg body weight (BW) in saline per day, respectively, for 10 days. Growth rate and food conversion efficiency were reduced (p<0.05) in the DSS piglets compared with the control group. Quantitative histopathological grading of inflammation in the jejunum and colon collectively showed that the DSS treatment resulted in 12 fold greater (p<0.05) inflammation severity scoring in the colon than in the jejunum, indicative of chronic ulcerative colitis in the colon. Upper gut permeability endpoint was 27.4 fold higher (p<0.05) in the DSS group compared with the control group. The DSS group had higher concentrations and mRNA abundances (p<0.05) of TNF- and IL-6 in the jejunal and colonic tissues compared with the control group. Colonic concentration and mRNA abundance of IL-10 were reduced (p<0.05), however, jejunal IL-10 mRNA abundance was increased (p<0.05) in the DSS group compared with the control group. In conclusion, administration of DSS at 1.25 g/kg BW for 10 days respectively induced acute inflammation in the jejunum and chronic inflammation and ulcerative colitis in the colon with substantially decreased colonic concentration and mRNA abundance of IL-10 in the young pigs, mimicking the IL-10 expression pattern in humans associated with chronic bowel inflammation.

scholarly journals A Novel Combination Therapy Using Rosuvastatin and Lactobacillus Combats Dextran Sodium Sulfate-Induced Colitis in High-Fat Diet-Fed Rats by Targeting the TXNIP/NLRP3 Interaction and Influencing Gut Microbiome Composition

2021 ◽  
Vol 14 (4) ◽  
pp. 341
Author(s):  
Sameh Saber ◽  
Eslam E. Abd El-Fattah ◽  
Galal Yahya ◽  
Naglaa A. Gobba ◽  
Abdalkareem Omar Maghmomeh ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Nlrp3 Inflammasome ◽  
Sodium Sulfate ◽  
High Fat Diet ◽  
Intestinal Inflammation ◽  
Dextran Sodium Sulfate ◽  
Ldl Oxidation ◽  
Ros Generation ◽  
Inflammasome Activation ◽  
High Fat

Inflammasome targeting and controlling dysbiosis are promising therapeutic approaches to control ulcerative colitis. This report is the first to investigate the mechanisms underlying the coloprotective effects of rosuvastatin and Lactobacillus and their combined therapy on dextran sodium sulfate (DSS)-induced colitis in high-fat diet (HFD)-fed rats. Our results demonstrate the aggravation of intestinal inflammation as a consequence of an HFD following DSS administration. An association between dyslipidemia, LDL oxidation, CD36 expression, ROS generation, thioredoxin-interacting protein (TXNIP) upregulation, and NLRP3 inflammasome activation was demonstrated by DSS exposure in HFD-fed rats. We demonstrated that rosuvastatin/Lactobacillus significantly suppressed the DSS/HFD-induced increase in colon weight/length ratio, DAI, MDI, and myeloperoxidase, as well as corrected dysbiosis and improved histological characteristics. Additionally, caspase-1 activity and IL-1β-driven pyroptotic activity was significantly reduced. Rosuvastatin/Lactobacillus showed prominent anti-inflammatory effects as revealed by the IL-10/IL-12 ratio and the levels of TNF-α and IL-6. These latter effects may be attributed to the inhibition of phosphorylation-induced activation of NF-κB and a concomitant reduction in the expression of NLRP3, pro-IL-1β, and pro-IL-18. Furthermore, rosuvastatin/Lactobacillus reduced Ox-LDL-induced TXNIP and attenuated the inflammatory response by inhibiting NLRP3 inflammasome assembly. To conclude, rosuvastatin/Lactobacillus offers a safe and effective strategy for the management of ulcerative colitis.

Increased expression of lipocalin-type-prostaglandin D synthase in ulcerative colitis and exacerbating role in murine colitis

2011 ◽  
Vol 300 (3) ◽  
pp. G401-G408 ◽  
Author(s):  
Ryota Hokari ◽  
Chie Kurihara ◽  
Nanae Nagata ◽  
Kosuke Aritake ◽  
Yoshikiyo Okada ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Disease Activity ◽  
Mrna Expression ◽  
Sodium Sulfate ◽  
Intestinal Inflammation ◽  
Dextran Sodium Sulfate ◽  
Muscularis Mucosa ◽  
Murine Colitis ◽  
Prostaglandin D Synthase ◽  
Cox 2

The pathogenesis of ulcerative colitis (UC) is unclear, but enhancement of disease activity by usage of nonsteroidal anti-inflammatory drugs suggests involvement of prostanoid in its pathophysiology. However, biological effect of prostaglandin (PG) D2 on intestinal inflammation remains unknown. We investigated the expression of enzymes for PGD2 synthesis, prostaglandin D synthase (PGDS), and its relation to the activity of colitis in UC patients. The role of lipocalin-type PGDS (L-PGDS) using a murine colitis model was also assessed. Tissue samples were obtained by colonic biopsies from patients with UC. Expression levels of mRNAs for L-PGDS and hematopoietic-type PGDS were investigated by quantitative RT-PCR. COX-2 and L-PGDS expression was investigated by immunohistochemistry. Localization of L-PGDS expression was also determined by in situ hybridization. In experimental study, mice were treated with dextran sodium sulfate in the drinking water to induce colitis. The degree of colonic inflammation was compared with L-PGDS−/− mice and control mice. The level of L-PGDS mRNA expression was increased in UC patients in parallel with disease activity. Colocalization of L-PGDS and cyclooxygenase (COX) 2 was observed in lamina proprial infiltrating cells and muscularis mucosa in UC patients. The level of hematopoietic PGDS mRNA expression did not differ from control mucosa. Dextran sodium sulfate treatment to L-PGDS−/− mice showed lower disease activity than control mice. We reported for the first time the presence of L-PGDS in the COX-2-expressing cells in the mucosa of active UC patients and that only L-PGDS increased with disease activity. An animal model study suggests that PGD2 derived from L-PGDS-expressing cells plays proinflammatory roles in colitis.

The Role of SPARC in Human Ulcerative Colitis and Murine Dextran Sodium Sulfate-Induced Colitis

2011 ◽  
Vol 140 (5) ◽  
pp. S-837
Author(s):  
Tomohisa Takagi ◽  
Yuji Naito ◽  
Wataru Aoi ◽  
Ryusuke Horie ◽  
Kazuhiko Uchiyama ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Sodium Sulfate ◽  
Dextran Sodium Sulfate

scholarly journals Anti-inflammatory Bifidobacterium strains prevent dextran sodium sulfate induced colitis and associated gut microbial dysbiosis in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Shashank Singh ◽  
Ruchika Bhatia ◽  
Pragyanshu Khare ◽  
Shikha Sharma ◽  
Sivasubramanian Rajarammohan ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Sodium Sulfate ◽  
Activity Index ◽  
Disease Activity Index ◽  
Dextran Sodium Sulfate ◽  
Raw 264.7 Cells ◽  
Spleen Weight ◽  
Lipocalin 2 ◽  
Weight Percentage ◽  
Microbial Dysbiosis

Abstract Crohn’s and ulcerative colitis are common inflammatory conditions associated with Inflammatory bowel disease. Owing to the importance of diet based approaches for the prevention of inflammatory gut conditions, the present study was aimed to screen the human isolates of Bifidobacterium strains based on their ability to reduce LPS-induced inflammation in murine macrophage (RAW 264.7) cells and to evaluate prioritized strains for their preventive efficacy against ulcerative colitis in mice. Twelve out of 25 isolated strains reduced the production of LPS-induced nitric oxide and inflammatory cytokines. Furthermore, three strains, B. longum Bif10, B. breve Bif11, and B. longum Bif16 conferred protection against dextran sodium sulfate induced colitis in mice. The three strains prevented shortening of colon, spleen weight, percentage body weight change and disease activity index relative to colitis mice. Lower levels of Lipocalin-2, TNF-α, IL-1β and IL-6 and improved SCFA levels were observed in Bifidobacterium supplemented mice relative to DSS counterparts. Bacterial composition of B. longum Bif10 and B. breve Bif11 fed mice was partly similar to the normal mice, while DSS and B. longum Bif16 supplemented mice showed deleterious alterations. At the genus level, Bifidobacterium supplementation inhibited the abundances of pathobionts such as Haemophilus, Klebsiella and Lachnospira there by conferring protection.

Therapeutic Effects of Ecabet Sodium, an Antiulcer Drug, on Dextran Sodium Sulfate–Induced Ulcerative Colitis in Rats

2005 ◽  
Vol 50 (5) ◽  
pp. 922-927 ◽  
Author(s):  
Tsunehisa Noto ◽  
Hiroshi Yamada ◽  
Takashi Inui ◽  
Kayoko Okuyama ◽  
Ayako Watanable ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Sodium Sulfate ◽  
Dextran Sodium Sulfate ◽  
Therapeutic Effects ◽  
Antiulcer Drug ◽  
Ecabet Sodium

scholarly journals Production of lipid mediators across different disease stages of dextran sodium sulfate-induced colitis in mice

2018 ◽  
Vol 59 (4) ◽  
pp. 586-595 ◽  
Author(s):  
Taiki Hamabata ◽  
Tatsuro Nakamura ◽  
Sakura Masuko ◽  
Shingo Maeda ◽  
Takahisa Murata
Keyword(s):  
Fatty Acid ◽  
Sodium Sulfate ◽  
Acute Inflammation ◽  
Intestinal Inflammation ◽  
Recovery Phase ◽  
Lipid Mediators ◽  
Dextran Sodium Sulfate ◽  
Prostaglandin E ◽  
Induction Phase ◽  
Colon Tissue

Although several studies have revealed the role of different lipid mediators in colitis, the comprehensive analysis of their production across different phases of colitis remained unclear. Here, we performed the following analysis in the dextran sodium sulfate (DSS)-induced colitis model using LC-MS/MS. Oral administration of 2% DSS in mice for 4 days resulted in severe intestinal inflammation by day 7, which gradually subsided by day 18. Based on the disease scoring index (assigned on the basis of fecal condition and weight loss), we defined the phases of colitis as induction (days 0–4), acute inflammation (days 4–7), recovery (days 7–9), and late recovery (days 9–18). Across all phases, 58 lipid mediators were detected in the inflamed colon tissue. In the induction phase, the production of n-6 fatty acid-derived prostaglandin E2 and thromboxane B2 increased by ∼2-fold. In the acute inflammation phase, the production of n-6 fatty acid-derived leukotrienes increased by >10-fold, while that of n-3 fatty acid-derived hydroxyeicosapentaenoic acids and dihydroxyeicosatetraenoic acids decreased. In the recovery phase, a precursor of protectin D1 (17-hydroxydocosahexaenoic acid) increased over 3-fold. These observations suggested dynamic changes in the production of lipid mediators across different phases of the disease and their potential regulation in healing colitis.

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