Effects of the anti‐ICAM‐1 monoclonal antibody on dextran sodium sulphate‐induced colitis in rats

Taniguchi, Takao; Tsukada, Hideaki; Nakamura, Hiroshi; Kodama, Mitsuo; Fukuda, Kazuhito; Saitō, Tsunemasa; Miyasaka, Masayuki; Seino, Yutaka

doi:10.1111/j.1440-1746.1998.tb00766.x

Cited by 83 publications

(63 citation statements)

References 12 publications

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“…ICAM-1 plays a vital role in this inflammatory setting. 36 Our data demonstrate differentially increased TNF-␣ expression in Sdc1 KO mice during DSS colitis. Stimulation of epithelial cells with the proinflammatory cytokine TNF-␣ induces Sdc1 downregulation and results in its shedding after cleavage by matrix metalloproteinases, thereby enhancing cellular migration.…”

Section: Sdc1 and Dss Colitismentioning

confidence: 75%

Enoxaparin Improves the Course of Dextran Sodium Sulfate-Induced Colitis in Syndecan-1-Deficient Mice

Floer

Götte

Wild

et al. 2010

The American Journal of Pathology

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Syndecan-1 (Sdc1) plays a major role in wound healing and modulates inflammatory responses. Sdc1 expression is reduced in lesions of patients with ulcerative colitis. The aim of this study was to investigate the role of Sdc1 in murine dextran sodium sulfate (DSS)-induced colitis. DSS colitis was induced in Sdc1-deficient (knockout (KO)) and wild-type mice by oral administration of 3% DSS. KO mice exhibited a significantly increased lethality as compared with wild-type controls (61 versus 5% , P < 0.05). Impaired mucosal healing and prolonged recruitment of inflammatory cells in KO mice were accompanied by significant up-regulation of tumor necrosis factor-␣, CC chemokine ligand 3/macrophage inflammatory protein-1␣, and vascular cell adhesion molecule-1 , as determined by histological correlation between 0 and 15 days after colitis induction , TaqMan low-density array analysis , and quantitative real-time PCR. Treatment from days 7 through 14 with enoxaparin , a functional analogue of the Sdc1 heparan sulfate chains , significantly reduced lethality of KO mice due to DSS-induced colitis , which was correlated with improved mucosal healing. In vitro, Sdc1-deficient polymorphonuclear cells displayed increased adhesion to endothelial cells and intercellular adhesion molecule-1, and enoxaparin reverted adhesion to wild-type levels. Small interfering RNA-mediated knockdown of Sdc1 expression resulted in reduced basic fibroblast growth factor-mediated mitogen-activated protein kinase signaling and reduced Caco-2 cell proliferation. We conclude that Sdc1 has a protective effect during experimental colitis. The modification of missing Sdc1 function by heparin analogues may emerge as a promising anti-inflammatory approach. (Am J Pathol

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Section: Sdc1 and Dss Colitismentioning

confidence: 75%

Enoxaparin Improves the Course of Dextran Sodium Sulfate-Induced Colitis in Syndecan-1-Deficient Mice

Floer

Götte

Wild

et al. 2010

The American Journal of Pathology

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“…Three lines of evidence sup- [35], 2) selective depletion of neutrophils by monoclonal antibody RP-3 suppresses colitis in rats [36], and 3) immunoneutralization of ICAM-1 on endothelial cells significantly attenuated colonic mucosal injury and neutrophil accumulation [37].…”

Section: Discussionmentioning

confidence: 99%

Effect of a Novel Water-Soluble Vitamin E Derivative, 2-(.ALPHA.-D-Glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol, on Dextran Sulfate Sodium-Induced Colitis in Mice

Naito

Takagi

Matsuyama

et al. 2002

J. Clin. Biochem. Nutr.

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“…Dextran sulfate sodium (DSS) colitis was induced by adding DSS to the drinking water, as previously described (Umene et al, 1994;Taniguchi et al, 1998;Wu and Ling, 1998;Soriano et al, 2000) (n ϭ 9) and DSS ϩ pravastatin (n ϭ 9) groups were administered 3% (w/v) DSS (molecule mass 44 kDa; TdB Consultancy AB, Uppsala, Sweden) in distilled water ad libitum. Control (n ϭ 9) and pravastatin (n ϭ 9) groups received distilled water without DSS.…”

Section: Methodsmentioning

confidence: 99%

The 3-Hydroxy-3-methylglutaryl-CoA Reductase Inhibitor Pravastatin Reduces Disease Activity and Inflammation in Dextran-Sulfate Induced Colitis

Sasaki

Bharwani²,

Jordan³

et al. 2003

J Pharmacol Exp Ther

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The dextran sulfate (DSS) model of colitis causes intestinal injury sharing many characteristics with inflammatory bowel disease, e.g., leukocyte infiltration, loss of gut epithelial barrier, and cachexia. These symptoms are partly mediated by entrapped leukocytes binding to multiple endothelial adhesion molecules (MAdCAM-1, VCAM-1, ICAM-1, and E-selectin). Pravastatin, an 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor, has anti-inflammatory potency in certain inflammation models; therefore, in this study, we measured the effects of pravastatin in DSS-induced colitis. The administration of pravastatin (1 mg/kg) relieved DSS-induced cachexia, hematochezia, and intestinal epithelial permeability, with no effect on serum cholesterol. Histopathologically, pravastatin prevented leukocyte infiltration and gut injury. Pravastatin also blocked the mucosal expression of MAdCAM-1. DSS treatment promoted mucosal endothelial nitric-oxide synthase (eNOS) mRNA degradation, an effect that was blocked by pravastatin. Importantly, the protective effects of pravastatin in DSS-induced colitis were not found in eNOS-deficient mice. Our results demonstrate that HMG-CoA reductase inhibitors preserve intestinal integrity in colitis, most likely via increased eNOS expression and activity, independent of cholesterol metabolism.Inflammatory bowel disease (IBD) (Crohn's colitis and ulcerative colitis) is characterized by tissue edema, increased gut epithelial permeability, and extensive infiltration of the gut by leukocytes. The general morbidity and weight loss in individuals with IBD can be attributed to leukocyte sequestration in the gut in this condition (Perkal and Seashore, 1989;Shanahan, 2002). The current literature suggests that multiple immune, genetic, and environmental factors influence both the initiation and progression of colitis (Farrell and Peppercorn, 2002). Despite the fact that the normal intestinal mucosa maintains a high density of leukocytes compared with most tissues, it is not typically inflamed or edematous. However, during active periods of colitis, the colon is even more extensively colonized by lymphocytes and neutrophils that promote extensive oxidant and protease-dependent injury to the gut. Therefore, it is assumed that the intestine has several specialized mechanisms that normally contain these immune responses and that the impairment of these immune-limiting processes causes the entrapment and activation of leukocytes seen in IBD injury. Among the several endogenous agents that control inflammation, nitric oxide has received a great deal of interest as a factor that can limit forms of inflammation. Endothelial cells release nitric oxide (NO) through both by the "constitutive" (eNOS and NOS3) and inducible nitric oxide synthases (iNOS and NOS1). NO released by microvascular endothelial cells reduces several indices of inflammation in vivo and in vitro. NO is a potent reactive oxygen species scavenger and can block many oxidant-mediated inflammatory responses including leukocyte and platel...

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Effects of the anti‐ICAM‐1 monoclonal antibody on dextran sodium sulphate‐induced colitis in rats

Cited by 83 publications

References 12 publications

Enoxaparin Improves the Course of Dextran Sodium Sulfate-Induced Colitis in Syndecan-1-Deficient Mice

Enoxaparin Improves the Course of Dextran Sodium Sulfate-Induced Colitis in Syndecan-1-Deficient Mice

Effect of a Novel Water-Soluble Vitamin E Derivative, 2-(.ALPHA.-D-Glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol, on Dextran Sulfate Sodium-Induced Colitis in Mice

The 3-Hydroxy-3-methylglutaryl-CoA Reductase Inhibitor Pravastatin Reduces Disease Activity and Inflammation in Dextran-Sulfate Induced Colitis

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