Molecular association of trinitrobenzenesulfonic acid and surface phospholipids in the development of colitis in rats

Tatsumi, Yoshihide; Lichtenberger, Lenard M.

doi:10.1053/gast.1996.v110.pm8608888

Cited by 27 publications

(23 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…To our knowledge, this is the first time that the ingestion of SCF reduced the systemic endotoxin concentration in TNBS colitis rats. It has been shown that TNBS itself deteriorates mucosal barrier function by interacting with surface-active phospholipids of the colonic mucosa [3]. Shortly after intracolonic administration, TNBS reduces surface hydrophobicity and increases tissue susceptibility to bacteria and endotoxin, leading to an inflammatory cascade, including the release of inflammatory cytokines such as IL-1b, IL-6, and tumor necrosis factor (TNF)-a [6,9].…”

Section: Discussionmentioning

confidence: 99%

“…The colitis is also partly due to the induction of an interleukin (IL)-12-driven inflammation with a Th1-mediated response to TNBS-modified proteins [3][4][5]. In rats, however, the inflammation pattern of the acute phase of colitis, at 1-2 weeks after TNBS administration, has been shown to resemble nonspecific colitis induced by intracolonic acetic acid administration [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Short-Chain Inulin-Like Fructans Reduce Endotoxin and Bacterial Translocations and Attenuate Development of TNBS-Induced Colitis in Rats

et al. 2008

View full text Add to dashboard Cite

Anti-inflammatory effects of short-chain inulin-like fructans (SCF) on trinitrobenzene sulfonic acid (TNBS)-induced colitis were investigated in rats, focusing specifically on endotoxin and bacterial translocations. SCF with degrees of polymerization (DP) of 4 and 8 were used. Rats were fed either control diet or diets including 60 g DP4 or DP8 per kilogram for 7 days, and then received intracolonic TNBS and were fed the respective diets for a further 10 days. DP4 and DP8 significantly reduced colonic injuries as assessed by damage score, but the reduction of colonic myeloperoxidase activity was manifest solely with DP8. At 3 days after colitis induction, bacterial translocation to the mesenteric lymph node was significantly lower in the DP4 and DP8 groups, but significant reduction in the portal endotoxin concentration was achieved solely in the DP8 group. Immediately prior to colitis induction, cecal immunoglobulin A and mucin concentrations were higher in the DP4 and DP8 groups, but these changes were abolished at 10 days post colitis induction. The data suggest that SCF exert prophylactic effects against TNBS colitis, presumably as a result of inhibitory effects on endotoxin and bacterial translocations.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Short-Chain Inulin-Like Fructans Reduce Endotoxin and Bacterial Translocations and Attenuate Development of TNBS-Induced Colitis in Rats

et al. 2008

View full text Add to dashboard Cite

show abstract

“…TNBS may reduce mucosal hydrophobicity by reacting with the surface-active phospholipids of the colonic mucosa. Reduced hydrophobic integrity of the colonic mucosa may contribute to TNBS-induced colonic inflammation (Tatsumi and Lichtenberger, 1996). TNBS causes necrosis and deeper tissue damage (somewhat akin to transmural inflammation seen in CD).…”

Section: Tnbsmentioning

confidence: 99%

Animal Models of Colitis: Lessons Learned, and Their Relevance to the Clinic

Barnett¹,

Fraser²

2011

Ulcerative Colitis - Treatments, Special Populations and the Future

View full text Add to dashboard Cite

“…(TNF-!) and interleukin-6 (IL-6) (11), tissue granulocyte accumulation, elevated extents of nitric oxide (NO) and peroxynitrite formation (12,13), weight loss (14), and mucosal barrier damage (15). As a consequence of inflammation, a mucosal microcirculatory dysfunction develops with leukocyte recruitment and extravasation, which is followed by the formation of large amounts of oxygen radicals (16) and oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Dietary Phosphatidylcholine Supplementation Attenuates Inflammatory Mucosal Damage in a Rat Model of Experimental Colitis

Kovács¹,

Varga

Érces

et al. 2012

Shock

View full text Add to dashboard Cite

This study was designed to follow the time course of inflammatory activation in a rodent model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. We hypothesized that oral phosphatidylcholine (PC) pretreatment regimens may influence leukocyte-mediated microcirculatory reactions in this condition. In series I, Wistar rats were monitored 1 day after colitis induction (n = 24), and in series II (n = 24) on day 6 following a TNBS enema. The PC-pretreated animals received a 2% PC-enriched diet for 6 days before the TNBS enema (series I), or for 3 days before and 3 days after TNBS treatment (series II). The macrohemodynamics, serosal microcirculation (visualized by intravital videomicroscopy), colonic xanthine oxidoreductase, myeloperoxidase and nitric oxide end products, and changes in proinflammatory cytokine levels in plasma were measured. The mucosal structural injury was monitored in vivo by means of confocal laser scanning endomicroscopy. The TNBS enema induced a systemic hyperdynamic circulatory reaction with increased serosal capillary blood flow and significantly elevated colonic inflammatory enzyme activities, levels of nitric oxide production, and cytokine concentrations. Acute colitis caused disruption of the capillary network, whereas the morphologic damage was less severe in series II. The PC pretreatment protocols led to significant decreases in the serosal hyperemic reaction, the cytokine levels, and the inflammatory enzyme activities. The objective signs of tissue damage were reduced in both series, and the number of mucus-producing goblet cells in the resolving phase of colitis was increased. Dietary PC efficiently decreases the cytokine-mediated progression of inflammatory events and preserves the microvascular structure in the large intestine.

show abstract

Molecular association of trinitrobenzenesulfonic acid and surface phospholipids in the development of colitis in rats

Cited by 27 publications

References 1 publication

Short-Chain Inulin-Like Fructans Reduce Endotoxin and Bacterial Translocations and Attenuate Development of TNBS-Induced Colitis in Rats

Short-Chain Inulin-Like Fructans Reduce Endotoxin and Bacterial Translocations and Attenuate Development of TNBS-Induced Colitis in Rats

Animal Models of Colitis: Lessons Learned, and Their Relevance to the Clinic

Dietary Phosphatidylcholine Supplementation Attenuates Inflammatory Mucosal Damage in a Rat Model of Experimental Colitis

Contact Info

Product

Resources

About