Bacterial Lipopolysaccharide and Tumor Necrosis Factor Alpha Synergistically Increase Expression of Human Endothelial Adhesion Molecules through Activation of NF-κB and p38 Mitogen-Activated Protein Kinase Signaling Pathways

Jersmann, Hubertus; Hii, Charles S.; Ferrante, Judith; Fèrrante, Antonio

doi:10.1128/iai.69.3.1273-1279.2001

Cited by 98 publications

(92 citation statements)

References 37 publications

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“…It was claimed that the LPS-induced expression of adhesion molecules CD11b/CD18 in neutrophils was related to the translocation of CD11b/ CD18 from secretory vesicles and specific granules to the plasma membrane [10] as well as the conformation change in I-domain, the active region of CD11b/CD18 in neutrophils [31][32][33] . On the other hand, the expression of adhesion molecules ICAM-1 in endothelial cells was modulated by NF-κB [34] , and conformation change in I-domain in endothelial cells [30,35,36] . Previous in vitro studies demonstrated that aqueous extract of Danshen, the main ingredients of compound Danshen injection, inhibited the expression of ICAM-1 and activation of NF-κB in endothelial cells [19,20] .…”

Section: Discussionmentioning

confidence: 99%

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Han

Horie²,

Miura³

et al. 2007

WJG

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stained with Monastral blue B, rolling and adhesion of leukocytes, production of oxygen radical in venular wall, albumin efflux and enhanced mast cell degranulation in vivo , all of which, except for the leukocyte rolling, were attenuated by the treatment with compound Danshen injection. Experiments performed in vitro further revealed that the expression of CD11b/CD18 and the production of oxygen free radical in neutrophils, and the expression of ICAM-1 in HUVECs were increased by exposure to LPS, and they were attenuated by compound Danshen injection. CONCLUSION: These results suggest that compoundDanshen injection is an efficient drug with multi-targeting potential for improving the microcirculatory disturbance. INTRODUCTIONIt is now well-recognized that stimulation with lipopolysaccharide (LPS) leads to a number of responses in microcirculation, such as endothelial cell damage, an increase in rolling, adhesion and emigration of leukocytes in post-capillary venules, enhanced oxygenfree radical production, mast cell degranulation and protein efflux [1][2][3][4][5][6] . Furthermore, it is demonstrated that LPS stimulation evokes an increase in the expression of adhesion molecules, including L-selectin [7] and CD11b/CD18 in leukocytes, E-selectin and intercellular adhesion molecule 1 (ICAM-1) in endothelial cells [7][8][9][10][11][12][13] . In addition, LPS stimulation can cause the release of proinflammatory mediators and vasoactive substances, such Abstract AIM: To investigate the effect of compound Danshen injection on lipopolysaccharide (LPS)-induced rat mesenteric microcirculatory dysfunctions and the underlying possible mechanism by an inverted intravital microscope and high-speed video camera system. METHODS:LPS was continuously infused through the jugular artery of male Wistar rats at the dose of 2 mg/kg per hour. Changes in mesenteric microcirculation, such as diameters of arterioles and venules, velocity of RBCs in venules, leukocyte rolling, adhesion and emigration, free radicals released from post-capillary venules, FITCalbumin leakage and mast cell degranulation, were observed through an inverted intravital microscope assisted with CCD camera and SIT camera. Meanwhile, the expression of adhesion molecules CD11b/CD18 and the production of free radical in neutrophils, and the expression of intercellular adhesion molecule 1 (ICAM-1) in human umbilical vein endothelial cells (HUVECs) were quantified by flow cytometry (FACS) in vitro . RESULTS:The continuous infusion with LPS resulted in a number of responses in microcirculation, including a significant increase in the positive region of venule

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Section: Discussionmentioning

confidence: 99%

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Han

Horie²,

Miura³

et al. 2007

WJG

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“…LPS can be recognized by monocytes, macrophages, neutrophils, and endothelial cells in mammals. Especially in endothelial cells, LPS induces adhesion molecule expression [8]. The most important of the adhesion molecules involved in this process are intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin [8,9].…”

Section: Introductionmentioning

confidence: 99%

“…Especially in endothelial cells, LPS induces adhesion molecule expression [8]. The most important of the adhesion molecules involved in this process are intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin [8,9]. Without stimulation, only a small amount of ICAM-1 is present on the endothelial cell surface [10], and VCAM-1 and E-selectin are absent entirely [11,12], but they are immediately expressed in response to extracellular inflammatory stimulation [13].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Lipopolysaccharide Activity by a Bacterial Cyclic Lipopeptide Surfactin

et al. 2006

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Compounds that inactivate lipopolysaccharide (LPS) activity have the potential of being new antiinflammatory agents. Therefore, we searched among microbial secondary metabolites for compounds that inhibited LPS-stimulated adhesion between human umbilical vein endothelial cells (HUVEC) and HL-60 cells. By this screening, we found a cyclic lipopeptide surfactin from the culture broth of Bacillus sp. BML752-121F2 to be inhibitory. The addition of the surfactin prior to the LPS stimulation decreased HL-60 cell-HUVEC adhesion without showing any cytotoxicity. We confirmed that surfactin inhibited LPS-induced expression of ICAM-1 and VCAM-1 in HUVEC. It also inhibited the cellular adhesion induced by lipid A, the active component of LPS; but it did not inhibit TNF-a or IL-1b -induced cell adhesion. Then, surfactin was shown to suppress the interaction of lipid A with LPS-binding protein (LBP) that mediates the transport of LPS to its receptors. Finally, surface plasmon resonance (SPR) analysis revealed the surfactin to interact reversibly with lipid A. Thus, this Bacillus surfactin was shown to be an inhibitor of LPS-induced signal transduction, directly interacting with LPS.

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“…The promoter of both ICAM-1 and VCAM-1 genes contains nuclear factor κB (NFκB) binding sites, and it has been shown that NFκB activation is necessary for TNFα-induced expression of ICAM-1 and VCAM-1 (5)(6)(7)(8)(9). It is generally believed that mitogen-activated protein (MAP) kinases are upstream of NFκB.…”

Section: Introductionmentioning

confidence: 99%

p38 Kinase and c‐Jun N‐Terminal Kinase Oppositely Regulates Tumor Necrosis Factor α‐Induced Vascular Cell Adhesion Molecule‐1 Expression and Cell Adhesion in Chondrosarcoma Cells

Kim

Jun

et al. 2002

IUBMB Life

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Bacterial Lipopolysaccharide and Tumor Necrosis Factor Alpha Synergistically Increase Expression of Human Endothelial Adhesion Molecules through Activation of NF-κB and p38 Mitogen-Activated Protein Kinase Signaling Pathways

Cited by 98 publications

References 37 publications

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Inhibition of Lipopolysaccharide Activity by a Bacterial Cyclic Lipopeptide Surfactin

p38 Kinase and c‐Jun N‐Terminal Kinase Oppositely Regulates Tumor Necrosis Factor α‐Induced Vascular Cell Adhesion Molecule‐1 Expression and Cell Adhesion in Chondrosarcoma Cells

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