Role of cell adhesion molecules in leukocyte recruitment in the liver and gut

Ala, Aftab; Dhillon, A. P.; Hodgson, H. J. F.

doi:10.1046/j.1365-2613.2003.00235.x

Cited by 69 publications

(53 citation statements)

References 84 publications

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“…Several lines of evidence have been proposed for the exact mechanisms involved in the development of IRI; however, the exact underlying mechanisms remain unclear [24]. Disturbance of the hepatic microcirculation [43] combined with cellular interaction between platelets [44], leukocytes [45], and endothelial lining cells [46], various Kupffer cell-derived proinflammatory mediators such as TNF-a, interleukin-1, and free radicals [47,48], and the expression of adhesion molecules are important determinants of the pathophysiologic changes that happen during IRI [24,49,50]. In the present study Kupffer cells showed enhanced capacity for phagocytosis of latex beads after CO 2 pneumoperitoneum.…”

Section: Discussionmentioning

confidence: 99%

Signs of reperfusion injury following CO2 pneumoperitoneum: an in vivo microscopy study

et al. 2007

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Section: Discussionmentioning

confidence: 99%

Signs of reperfusion injury following CO2 pneumoperitoneum: an in vivo microscopy study

et al. 2007

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“…14-16 Membranous ICAM-1 and VCAM-1 and transmembrane protein Eselectin mediate adhesion and interactions between cells or a cell and extracellular matrix 17 ; thus, their expression levels were determined. Ox-LDL treatment induced intensive membrane fluorescence, suggesting the increased membrane expression of ICAM-1, VCAM-1, and E-selectin, which was significantly inhibited by CPT, NAC, or BAY117082 pretreatment (Fig.…”

Section: Cpt Inhibited Ox-ldl-induced Membrane Adhesion Molecule Exprmentioning

confidence: 99%

Cryptotanshinone inhibits oxidized LDL-induced adhesion molecule expression via ROS dependent NF-κB pathways

Zhao

Chen

2016

Cell Adhesion & Migration

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Adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin, play important roles in the initial stage of atherosclerosis. Cryptotanshinone (CPT), a natural compound isolated from Salvia miltiorrhiza Bunge, exhibits antiatherosclerotic activity although the underlying mechanisms remain elusive. In this study, the protective effect of CPT against oxidized low-density lipoprotein (ox-LDL)-induced adhesion molecule expression was investigated in human umbilical vein endothelial cells. Ox-LDL significantly induced ICAM-1, VCAM-1, and E-selectin expression at the mRNA and protein levels but reduced eNOS phosphorylation and NO generation, which were reversed by CPT pretreatment. Sodium nitroprusside, a NO donor, N-acetyl-L-cysteine (NAC), a reactive oxygen species (ROS) scavenger, and BAY117082, a NF-kB inhibitor, inhibited ox-LDL-induced ICAM-1, VCAM-1, and Eselectin expression. Ox-LDL-induced ROS production was significantly inhibited by CPT and NAC. Furthermore, ox-LDL activated the NF-kB signaling pathway by inducing phosphorylation of IKKb and IkBa, promoting the interaction of IKKb and IkBa, and increasing p65 nuclear translocation, which were significantly inhibited by CPT. In addition, CPT, NAC, and BAY117082 inhibited ox-LDLinduced membrane expression of ICAM-1, VCAM-1, E-selectin, and endothelial-monocyte adhesion and restored eNOS phosphorylation and NO generation. Results suggested that CPT inhibited ox-LDL-induced adhesion molecule expression by decreasing ROS and inhibiting the NF-kB pathways, which provides new insight into the anti-atherosclerotic mechanism of CPT.

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“…Endothelial cell activation and surface upregulation of selectins are necessary parts in the localization of leukocytes at sites of tissue injury (2). Indeed, numerous studies have shown that P-, E-, and L-selectin support early interactions between leukocytes and endothelial cells at sites of inflammation (13,19,21,28).…”

Section: Discussionmentioning

confidence: 99%

“…Upon activation, neutrophil stiffness increases, promoting mechanical sequestration of neutrophils in lung capillaries (20,34). It is widely held that leukocyte rolling is mediated by the selectin family of adhesion molecules, including P-, E-and L-selectins although their relative roles appear to be both tissue-and stimulus-dependent (2,28). Selectin ligands are complex glycoproteins and, in terms of selectin specificity and function, are poorly understood.…”

mentioning

confidence: 99%

Targeting CD162 protects against streptococcal M1 protein-evoked neutrophil recruitment and lung injury

Zhang

Song

Wang

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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Zhang S, Song L, Wang Y, Herwald H, Thorlacius H. Targeting CD162 protects against streptococcal M1 protein-evoked neutrophil recruitment and lung injury. Am J Physiol Lung Cell Mol Physiol 305: L756 -L763, 2013. First published September 13, 2013 doi:10.1152/ajplung.00220.2013.-Streptococcus pyogenes of the M1 serotype can cause streptococcal toxic shock syndrome and acute lung damage. CD162 is an adhesion molecule that has been reported to mediate neutrophil recruitment in acute inflammatory reactions. In this study, the purpose was to investigate the role of CD162 in M1 protein-provoked lung injury. Male C57BL/6 mice were treated with monoclonal antibody directed against CD162 or a control antibody before M1 protein challenge. Edema, neutrophil infiltration, and CXC chemokines were determined in the lung, 4 h after M1 protein administration. Fluorescence intravital microscopy was used to analyze leukocyte-endothelium interactions in the pulmonary microcirculation. Inhibition of CD162 reduced M1 proteinprovoked accumulation of neutrophils, edema, and CXC chemokine formation in the lung by Ͼ54%. Moreover, immunoneutralization of CD162 abolished leukocyte rolling and firm adhesion in pulmonary venules of M1 protein-treated animals. In addition, inhibition of CD162 decreased M1 protein-induced capillary trapping of leukocytes in the lung microvasculature and improved microvascular perfusion in the lungs of M1 protein-treated animals. Our findings suggest that CD162 plays an important role in M1 protein-induced lung damage by regulating leukocyte rolling in pulmonary venules. Consequently, inhibition of CD162 attenuates M1 protein-evoked leukocyte adhesion and extravasation in the lung. Thus, our results suggest that targeting the CD162 might pave the way for novel opportunities to protect against pulmonary damage in streptococcal infections. adhesion; chemokines; inflammation and leukocyte CLINICAL MANIFESTATIONS OF Streptococcus pyogenes infections vary from uncomplicated cases to severe and fatal conditions, such as streptococcal toxic shock syndrome (STSS), which is associated with a mortality exceeding 50% (7, 15). Despite significant investigative efforts, management of patients with STSS is largely restricted to antibiotics and supportive care, which is partly due to an incomplete understanding of the basic pathophysiology in STSS. S. pyogenes express several different virulence factors, including M proteins, of which there are more than 80 different serotypes described in the literature (15,26). The M1 serotype of Streptococcus pyogenes is most commonly linked to STSS (7). Numerous studies have documented that M1 protein is a powerful stimulator of innate immune cells, such as monocytes (26) and neutrophils (15). In addition, the M1 protein has the capacity to induce formation of cytokines (26), chemokines (9), and tissue factor (25), which all contribute to M1 protein-induced edema formation and tissue damage in the lung. Several studies have shown that lung failure is an insidious feature in STSS patie...

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Role of cell adhesion molecules in leukocyte recruitment in the liver and gut

Abstract: Summary. This article reviews the evidence that adhesion molecules are critical in leukocyte recirculation and pathogenesis of diseases affecting the closely related tissues of the liver and gut, which offer novel opportunities for treatment.

Cited by 69 publications

References 84 publications

Signs of reperfusion injury following CO2 pneumoperitoneum: an in vivo microscopy study

Signs of reperfusion injury following CO2 pneumoperitoneum: an in vivo microscopy study

Cryptotanshinone inhibits oxidized LDL-induced adhesion molecule expression via ROS dependent NF-κB pathways

Targeting CD162 protects against streptococcal M1 protein-evoked neutrophil recruitment and lung injury

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