Mechanisms underlying the anti-inflammatory actions of boswellic acid derivatives in experimental colitis

Anthoni, Christoph; Laukoetter, Mike G.; Rijcken, Emile; Vowinkel, Thorsten; Mennigen, Rudolf; Muller, Sam H; Senninger, N.; Russell, Janice; Jauch, Johann; Bergmann, Jochen; Granger, D. Neil; Krieglstein, C. F.

doi:10.1152/ajpgi.00562.2005

Cited by 105 publications

(61 citation statements)

References 31 publications

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“…The platelets we observe are also very transiently interacting mainly with the endothelium, whereas others have reported leukocyte-platelet interactions (4,22,23,51,52). One possible explanation for the discrepancy between our study and others could be the fact that we have studied postcapillary mucosal venules up to a diameter of 20 m, while others have investigated platelet behavior in venules of bigger size and only in the deeper gut wall (ϳ40 m in diameter).…”

Section: Discussioncontrasting

confidence: 93%

Lactobacillus reuteriprevents colitis by reducing P-selectin-associated leukocyte- and platelet-endothelial cell interactions

Schreiber¹,

Petersson²,

Phillipson³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Schreiber O, Petersson J, Phillipson M, Perry M, Roos S, Holm L. Lactobacillus reuteri prevents colitis by reducing P-selectin-associated leukocyte-and platelet-endothelial cell interactions. Am J Physiol Gastrointest Liver Physiol 296: G534 -G542, 2009. First published January 15, 2009 doi:10.1152/ajpgi.90470.2008.-Recent findings indicate that dextran sodium sulfate (DSS)-induced colitis is associated with a prothrombogenic phenotype, with P-selectin playing a major role in platelet recruitment. It has been suggested that probiotics may ameliorate colonic inflammation. We therefore investigated how treatment with Lactobacillus reuteri influenced P-selectin expression, leukocyte and platelet endothelial cell interactions, and colitis severity in DSS-treated rats. Rats were divided into the following four groups: nontreated, DSS treated (5% in drinking water for 9 days), L. reuteri, and L. reuteri and DSS treated. The rats were anesthetized with Inactin (120 mg/kg ip), and the dual radiolabeled monoclonal antibody technique was used to quantify P-selectin expression. Leukocyte-endothelial and platelet-endothelial cell interactions were studied in colonic venules with intravital microscopy. Colitis severity was assessed using a disease activity index. Disease activity index increased, as did the expression of P-selectin in the entire colon after DSS treatment, but both were reduced to control levels with L. reuteri pretreatment. The increased platelet-and leukocyte-endothelial cell interactions after DSS treatment were abolished by pretreatment with L. reuteri. L. reuteri protects against DSS-induced colitis in rats. The protection is associated with reduced P-selectin expression and a decrease in leukocyte-and plateletendothelial cell interactions.

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Section: Discussioncontrasting

confidence: 93%

Lactobacillus reuteriprevents colitis by reducing P-selectin-associated leukocyte- and platelet-endothelial cell interactions

Schreiber¹,

Petersson²,

Phillipson³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Seven-micrometer frozen sections were cut, and standard H&E staining was performed as described previously. 22 Severity of the colitis was assessed by an established scoring system as published before. 23 For immunohistochemical analysis, the following primary antibodies were used: Sdc1 (rat anti-mouse Sdc1 mAb clone 281-2, diluted 1/100 in PBS with 1% BSA; BD Pharmingen, Heidelberg, Germany), Sdc2 (rabbit-antimouse, diluted 1/50; Santa Cruz Biotechnology, Santa Cruz, CA), Sdc3 (rat-anti-mouse mAb clone 312607, diluted 1/50; R&D Systems, Wiesbaden, Germany), Sdc4 (ratanti-mouse clone KY/8.2, diluted 1/50; BD Pharmingen), F4/80 (rat-anti-mouse, clone BM8; eBioscience, San Diego, CA), CD4, CD8, and B220 (rat anti-mouse, clone C3T4 (CD4), clone 53-6.7 (CD8), and clone RA3-6B2 (B220), diluted 1/100; BD Pharmingen).…”

Section: Histological Examinationmentioning

confidence: 99%

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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“…From each region of the colon, four transverse slides were made, resulting in 16 slides for evaluation of colitis for each animal as described before (26). Histological inflammation was scored in a blinded fashion by a score introduced by Dieleman et al (9), considering the degree of inflammation, the vertical extent of inflammation, and the crypt damage score, related to the percentage of involvement in each single slide (1,9).…”

Section: Induction Of Inflammationmentioning

confidence: 99%

PECAM-1 (CD 31) mediates transendothelial leukocyte migration in experimental colitis

Rijcken¹,

Mennigen²,

Schaefer³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Transendothelial migration of circulating leukocytes into the colonic wall is a key step in the development of the inflammatory infiltrate in inflammatory bowel disease (IBD). The platelet-endothelial cell adhesion molecule-1 PECAM-1 (CD31) is expressed in the tight junction area of endothelial cells, where it is supposed to support the transmigration process. The aim of this study was to determine the role of PECAM-1 in experimental IBD and to show whether blockade of PECAM-1 has therapeutic effects. Chronic colitis was induced in female BALB/c mice by cyclic oral administration of dextran sodium sulfate (DSS) 3% (wt/vol). Expression of PECAM-1 was visualized by immunohistochemistry. In the treatment group animals received 1 mg/kg anti-PECAM-1 (2H8) ip daily starting on day 26. On day 30 leukocyte adhesion and migration was measured during N(2)O-isoflurane anesthesia in the distal colon by intravital microscopy. Disease activity index (DAI), histology, and MPO levels were compared with healthy and diseased controls. PECAM-1 was expressed in colitic mice. Chronic DSS colitis was characterized by a marked increase in rolling, adherent, and transmigrated leukocytes compared with healthy controls. Immunoblockade of PECAM-1 reduced leukocyte transmigration significantly and also diminished leukocyte rolling and sticking in an indirect manner. It also resulted in a significantly diminished DAI and MPO levels, as well as an amelioration of the histological inflammation score. PECAM-1 plays an important role in transendothelial leukocyte migration in DSS colitis. PECAM-1 could be a novel target for antibody-based treatment in IBD.

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Mechanisms underlying the anti-inflammatory actions of boswellic acid derivatives in experimental colitis

Abstract: . Mechanisms underlying the anti-inflammatory actions of boswellic acid derivatives in experimental colitis.

Cited by 105 publications

References 31 publications

Lactobacillus reuteriprevents colitis by reducing P-selectin-associated leukocyte- and platelet-endothelial cell interactions

Lactobacillus reuteriprevents colitis by reducing P-selectin-associated leukocyte- and platelet-endothelial cell interactions

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

PECAM-1 (CD 31) mediates transendothelial leukocyte migration in experimental colitis

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