A diet with lactosucrose supplementation ameliorates trinitrobenzene sulfonic acid-induced colitis in rats

2015 ◽  
Vol 6 (1) ◽  
pp. 161-171 ◽  
Author(s):  
Yan Zhou ◽  
Zheng Ruan ◽  
Xiaoli Zhou ◽  
Xiaoliu Huang ◽  
Hua Li ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Sulfonic Acid ◽  
Intestinal Inflammation ◽  
Trinitrobenzene Sulfonic Acid ◽  
Increased Risk ◽  
Chronic Intestinal Inflammation

Chronic intestinal inflammation contributes to an increased risk of colon cancer.

scholarly journals Mouse model of ulcerative colitis using trinitrobenzene sulfonic acid

2015 ◽  
Vol 10 (4) ◽  
pp. 860
Author(s):  
Irfan Ahmad Rather ◽  
Vivek K. Bajpai ◽  
Nam Gyeong-Jun
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Bowel Disease ◽  
Sulfonic Acid ◽  
Intestinal Inflammation ◽  
Cost Effective ◽  
Trinitrobenzene Sulfonic Acid ◽  
Clinical Presentations ◽  
Inflammatory Bowel

<p>Animal model of intestinal inflammation is of paramount significance that aids in discerning the pathologies underlying ulcerative colitis and Crohn’s disease, the two clinical presentations of inflammatory bowel disease. The 2,4,6-trinitrobenzene sulfonic acid (TNBS) colitis model represents one such intestinal inflammation-prototype that is generated in susceptible strains of mice through intra-rectal instillation of compound TNBS. In this paper, we demonstrate the experimental induction of TNBS-mediated colitis in a susceptible strain of ICR mice. This can be done by the following steps: a) acclimation, b) induction and c) observation. TNBS-mouse model provides the information in shortest possible time and simultaneously represents a cost effective and highly reproducible model method of studying the pathogenesis of inflammatory bowel disease.</p><p><strong>Video Clips</strong></p><p><a href="https://youtube.com/v/6MsuIGzH3uA">Acclimation and induction of TNBS</a>:          4.5 min</p><p><a href="https://youtube.com/v/ya66SNwoVag">Observation and drug administration</a>:      1.5 min</p>

scholarly journals Hapten-induced Colitis Is Associated with Colonic Patch Hypertrophy and T Helper Cell 2–Type Responses

1999 ◽  
Vol 189 (8) ◽  
pp. 1169-1180 ◽  
Author(s):  
Taeko Dohi ◽  
Kohtaro Fujihashi ◽  
Paul D. Rennert ◽  
Koichi Iwatani ◽  
Hiroshi Kiyono ◽  
...  
Keyword(s):  
Sulfonic Acid ◽  
Intestinal Inflammation ◽  
T Helper Cell ◽  
Trinitrobenzene Sulfonic Acid ◽  
Murine Models ◽  
T Helper ◽  
Mucosal Layer ◽  
Inflammatory Bowel ◽  
Ifn Γ ◽  
Tnbs Colitis

To investigate the potential involvement of T helper (Th)2-type responses in murine models of intestinal inflammation, we used trinitrobenzene sulfonic acid (TNBS)–hapten to induce inflammatory bowel disease in situations where Th1-type responses with interferon (IFN)-γ synthesis are either diminished or do not occur. Intracolonic administration of TNBS to either normal (IFN-γ+/+) or Th1-deficient IFN-γ knockout (IFN-γ−/−) BALB/c mice resulted in significant colitis. In IFN-γ−/− mice, crypt inflammation was more severe than in IFN-γ+/+ mice and was accompanied by hypertrophy of colonic patches with a lymphoepithelium containing M cells and distinct B and T cell zones resembling Peyer's patches. Hapten-specific, colonic patch T cells from both mouse groups exhibited a Th2 phenotype with interleukin (IL)-4 and IL-5 production. TNBS colitis in normal mice treated with anti–IL-4 antibodies or in IL-4−/− mice was less severe than in either IFN-γ+/+ or IFN-γ−/− mice. Our findings now show that the Th2-type responses in TNBS colitis are associated with colonic patch enlargement and inflammation of the mucosal layer and may represent a model for ulcerative colitis.

Role of serotonin in intestinal inflammation: knockout of serotonin reuptake transporter exacerbates 2,4,6-trinitrobenzene sulfonic acid colitis in mice

2009 ◽  
Vol 296 (3) ◽  
pp. G685-G695 ◽  
Author(s):  
Stephan C. Bischoff ◽  
Reiner Mailer ◽  
Oliver Pabst ◽  
Gisela Weier ◽  
Wanda Sedlik ◽  
...  
Keyword(s):  
Serotonin Reuptake ◽  
Sulfonic Acid ◽  
Intestinal Inflammation ◽  
Inflammatory Responses ◽  
Colonic Motility ◽  
Trinitrobenzene Sulfonic Acid ◽  
Targeted Deletion ◽  
Immune Mediated ◽  
Serotonin Reuptake Transporter

Serotonin (5-HT) regulates peristaltic and secretory reflexes in the gut. The serotonin reuptake transporter (SERT; SLC6A4), which inactivates 5-HT, is expressed in the intestinal mucosa and the enteric nervous system. Stool water content is increased and colonic motility is irregular in mice with a targeted deletion of SERT. We tested the hypotheses that 5-HT plays a role in regulating intestinal inflammation and that the potentiation of serotonergic signaling that results from SERT deletion is proinflammatory. Rectal installation of 2,4,6-trinitrobenzene sulfonic acid (TNBS) was used to induce an immune-mediated colitis, which was compared in SERT knockout mice and littermate controls. Intestinal myeloperoxidase and histamine levels were significantly increased, whereas the survival rate and state of health were significantly decreased in TNBS-treated mice that lacked SERT. Deletion of SERT thus increases the severity of TNBS colitis. These data suggest that 5-HT and its SERT-mediated termination play roles in intestinal immune/inflammatory responses in mice.

Leptin resistant Zucker rats with trinitrobenzene sulfonic acid colitis present a reduced inflammatory response but enhanced epithelial damage

2021 ◽  
Author(s):  
Belén Rivero-Gutiérrez ◽  
María Arredondo-Amador ◽  
Reyes Gámez-Belmonte ◽  
Fermin Sánchez de Medina ◽  
Olga Martínez-Augustin
Keyword(s):  
Alkaline Phosphatase ◽  
Inflammatory Response ◽  
Sulfonic Acid ◽  
Intestinal Inflammation ◽  
Zucker Rats ◽  
Trinitrobenzene Sulfonic Acid ◽  
Mrna Levels ◽  
Leptin Signaling ◽  
Epithelial Damage ◽  
Obese Zucker Rats

The role of leptin in the development of intestinal inflammation remains controversial, since proinflammatory and anti-inflammatory effects have been described. This study describes the effect of the absence of leptin signaling in intestinal inflammation. Experimental colitis was induced by intrarectal administration of trinitrobenzene sulfonic acid (TNBS) to lean and obese Zucker rats (n=10). Effects on inflammation and mucosal barrier were studied. Bacterial translocation and LPS concentration were evaluated together with colonic permeability to 4 kDa FITC-dextran. Obese Zucker rats showed a lower intestinal myeloperoxidase and alkaline phosphatase activity, reduced alkaline phosphatase sensitivity to levamisole, and diminished colonic expression of Nos2, Tnf and Il6, indicating attenuated intestinal inflammation, associated with attenuated STAT3, AKT and ERK signaling in the colonic tissue. S100a8 and Cxcl1 mRNA levels were maintained, suggesting that in the absence of leptin signaling neutrophil activation rather than infiltration is hampered. In spite of the lower inflammatory response, leptin resistance enhanced intestinal permeability, reflecting an increased epithelial damage. This was shown by augmented LPS presence in the portal vein of colitic obese Zucker rats, associated with induction of tissue non-specific alkaline phosphatase, LPS-binding protein and CD14 hepatic expression (involved in LPS handling). This was linked to decreased ZO-1 immunoreactivity in tight junctions and lower occludin expression. Our results indicate that obese Zucker rats present an attenuated inflammatory response to TNBS, but increased intestinal epithelial damage allowing the passage of bacterial antigens.

S1708 A Crucial Regulatory Role of Vav1 in Chronic Intestinal Inflammation and Colitis Associated Colon Cancer

2008 ◽  
Vol 134 (4) ◽  
pp. A-254
Author(s):  
Imke Atreya ◽  
Christoph Becker ◽  
Victor Tybulevicz ◽  
Peter R. Galle ◽  
Markus F. Neurath
Keyword(s):  
Colon Cancer ◽  
Intestinal Inflammation ◽  
Regulatory Role ◽  
Chronic Intestinal Inflammation

scholarly journals Colorectal Cancer in Inflammatory Bowel Disease

2018 ◽  
Vol 31 (03) ◽  
pp. 168-178 ◽  
Author(s):  
Peter Higgins ◽  
Ryan Stidham
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Detection Techniques ◽  
Clinical Scenarios ◽  
Increased Risk ◽  
Consensus Statements ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

AbstractPatients with inflammatory bowel disease (IBD) are at significantly increased risk of colorectal cancer (CRC), principally resulting from the pro-neoplastic effects of chronic intestinal inflammation. Epidemiologic studies continue to highlight the increased risk of CRC in IBD. However, the incidence has declined over the past 30 years, attributed to both successful CRC-surveillance programs and improved control of mucosal inflammation. Risk factors that further increase the risk of IBD-related CRC include disease duration, extent and severity, the presence of inflammatory pseudopolyps, coexistent primary sclerosing cholangitis, and a family history of CRC. All major professional societies agree that IBD-CRC surveillance should occur more frequently than in the general population. Yet, guidelines and consensus statements differ on the surveillance schedule and preferred method of surveillance. Improved sensitivity to previously “invisible” flat dysplastic lesions using high definition and chromoendoscopy methods has resulted in many guidelines abandoning requirements for random untargeted biopsies of the colon. While colonic dysplasia remains a worrisome finding, and several clinical scenarios remain best addressed by total proctocolectomy due to concerns of synchronous undetected lesions and the unpredictable tempo of progression to malignancy, better detection techniques have also increased opportunities for endoscopic resection of dysplastic lesions that can be clearly delineated. Finally, the expanding armamentarium of medical options in IBD, including anti-tumor necrosis factor and anti-adhesion biologic therapies, have substantially improved our ability to control severe inflammation and likely reduce the risk of CRC over time.

Risk of Neurodegenerative Diseases in Patients with Inflammatory Bowel Disease: A Nationwide Population-based Cohort Study

2021 ◽  
Author(s):  
Ga Hee Kim ◽  
Yeong Chan Lee ◽  
Tae Jun Kim ◽  
Eun Ran Kim ◽  
Sung Noh Hong ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Neurodegenerative Diseases ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Disease Risk ◽  
Population Based ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Nested Case Control ◽  
Chronic Intestinal Inflammation

Abstract Background and Aims Although recent studies have reported that inflammatory bowel disease [IBD] is associated with the development of neurodegenerative diseases via chronic intestinal inflammation and the gut-brain axis, there is insufficient evidence supporting this notion. The aim of this study was to determine the risk of neurodegenerative diseases including Parkinson’s disease [PD] and Alzheimer’s disease [AD] in patients with IBD. Methods Using the National Health Insurance Service data for the entire Korean population, we identified patients with IBD and controls from 2009 to 2011 and followed them up until 2017. We selected the controls in a 1:4 ratio based on age and sex for comparison with cases. Results Of 24 830 IBD patients and 99 320 non-IBD controls, 98 IBD patients and 256 controls developed PD, and 644 IBD patients and 2303 controls developed AD. The overall neurodegenerative disease risk was higher in IBD patients (PD: adjusted hazard ratio [HR], 1.56; 95% confidence interval [CI], 1.24-1.97; AD: adjusted HR, 1.14; 95% CI, 1.05-1.25). Younger IBD patients aged 40-65 years had a higher risk of PD compared with controls [adjusted HR, 2.34; 1.63-3.35]. In contrast, patients aged ≥65 years had an increased risk of AD compared with controls [adjusted HR, 1.14; 1.04-1.25]. In a nested case-control study of the IBD cohort, patients aged ≥65 years and the female sex were risk factors for AD, whereas living in an urban area was protective against AD. Conclusions The risk of neurodegenerative diseases was higher in IBD patients than in the non-IBD population.

scholarly journals New paradigms in chronic intestinal inflammation and colon cancer: role of melatonin

2011 ◽  
Vol 51 (1) ◽  
pp. 44-60 ◽  
Author(s):  
Virginia Motilva ◽  
Sofía García-Mauriño ◽  
Elena Talero ◽  
Matilde Illanes
Keyword(s):  
Colon Cancer ◽  
Intestinal Inflammation ◽  
Chronic Intestinal Inflammation

scholarly journals Antibodies to interleukin 12 abrogate established experimental colitis in mice.

1995 ◽  
Vol 182 (5) ◽  
pp. 1281-1290 ◽  
Author(s):  
M F Neurath ◽  
I Fuss ◽  
B L Kelsall ◽  
E Stüber ◽  
W Strober
Keyword(s):  
T Cells ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Murine Model ◽  
Cd4 T Cells ◽  
Intestinal Inflammation ◽  
Interleukin 12 ◽  
Trinitrobenzene Sulfonic Acid ◽  
Ifn Gamma ◽  
Chronic Intestinal Inflammation

In this study, we describe a novel murine model of chronic intestinal inflammation induced by the hapten reagent 2,4,6-trinitrobenzene sulfonic acid (TNBS). Rectal application of low doses of TNBS in BALB/c and SJL/J mice resulted in a chronic transmural colitis with severe diarrhea, weight loss, and rectal prolapse, an illness that mimics some characteristics of Crohn's disease in humans. The colon of TNBS-treated mice on day 7 was marked by infiltration of CD4+ T cells; furthermore, in situ polymerase chain reaction studies revealed high levels of interferon (IFN)-gamma mRNA in diseased colons. Isolated lamina propria (LP) CD4+ T cells from TNBS-treated mice stimulated with anti-CD3 and anti-CD28 antibodies exhibited a Th1 pattern of cytokine secretion: a 20-50-fold increase in IL-2 and IFN-gamma levels and a 5-fold decrease in IL-4 levels as compared with those of stimulated LP CD4+ T cells from control BALB/c mice. Administration of monoclonal anti-IL-12 antibodies to the TNBS-treated mice both early (at 5 d) and late (at 20 d) after induction of colitis led to a striking improvement in both the clinical and histopathological aspects of the disease and frequently abrogated the established colitis completely. Furthermore, LP CD4+ T cells isolated from anti-IL-12-treated mice failed to secrete IFN-gamma upon in vitro stimulation. In summary, the data demonstrate the pivotal role of IL-12 and IFN-gamma in a TNBS-induced murine model of chronic intestinal inflammation. Furthermore, they suggest the potential utility of anti-IL-12 antibodies in patients with Crohn's disease.

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