CD18 integrin and CD54-dependent neutrophil adhesion to cytokine-stimulated human hepatocytes

Nagendra, A; Mickelson, Judith K.; Smith, C. Wayne

doi:10.1152/ajpgi.1997.272.3.g408

Cited by 43 publications

(52 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…12 However, others have shown that pharmacological doses of IFN-␥ may produce anti-inflammatory effects, 18 consistent with our finding that INFRG KO mice suffered even more severe IRI damage than WT. Indeed, IFN-␥ may exert cytoprotective functions by modulating the production of proteases/reactive oxygen species from KC, 19 by decreasing CD54 20 or E/P selectin 21 expression. Although both IFNs stimulate the production of IFN-inducible proteins, 22 our results have revealed that type I IFN selectively mediated liver CXCL10 induction.…”

Section: Discussionmentioning

confidence: 99%

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion

et al. 2007

View full text Add to dashboard Cite

We have documented the key role of toll-like receptor 4 (TLR4) activation and its signaling pathway mediated by interferon (IFN) regulatory factor 3, in the induction of inflammation leading to the hepatocellular damage during liver ischemia/reperfusion injury (IRI). Because type I IFN is the major downstream activation product of that pathway, we studied its role in comparison with IFN-␥. Groups of type I (IFNAR), type II (IFNGR) IFN receptordeficient mice, along with wild-type (WT) controls were subjected to partial liver warm ischemia (90 minutes) followed by reperfusion (1-6 hours). Interestingly, IFNAR knockout (KO) but not IFNGR KO mice were protected from IR-induced liver damage, as evidenced by decreased serum alanine aminotransferase and preservation of tissue architecture. IRtriggered intrahepatic pro-inflammatory response, assessed by tumor necrosis factor (TNF-␣), interleukin 6 (IL-6), and chemokine (C-X-C motif) ligand 10 (CXCL-10) expression, was diminished selectively in IFNAR KO mice. Consistent with these findings, our in vitro cell culture studies have shown that: (1) although hepatocytes alone failed to respond to lipopolysaccharide (LPS), when co-cultured with macrophages they did respond to LPS via macrophage-derived IFN-␤; (2) macrophages required type I IFN to sustain CXCL10 production in response to LPS. This study documents that type I, but not type II, IFN pathway is required for IR-triggered liver inflammation/damage. Type I IFN mediates potential synergy between nonparenchyma and parenchyma cells in response to TLR4 activation. (HEPATOLOGY 2008;47:199-206.) L iver ischemia/reperfusion injury (IRI) occurs in multiple clinical settings including surgical interventions, trauma, and transplantation. 1-3 The mechanisms underlying liver IRI are complex but are known to involve interactions between both nonparenchyma cells, such as Kupffer cells (KC), and parenchyma cells, such as hepatocytes. Local leukocyte sequestration and activation (neutrophils, macrophages, and T cells) leads to the formation of reactive oxygen species, secretion of pro-inflammatory cytokines/chemokines, complement activation, and vascular cell adhesion molecule activation. Because IRI develops in the absence of exogenous antigens, it has been considered as an innate immune-mediated pro-inflammatory response.It was demonstrated that the mammalian sentinel tolllike-receptor (TLR) system plays a critical role in the development of IRI. 4-7 Indeed, TLR4 activation proved essential in the induction of inflammation in a warm liver IRI mouse model. In the absence of TLR4 but not TLR2 signaling, livers were protected from IRI, and intrahepatic induction of tumor necrosis factor (TNF-␣) and interleukin 1 (IL-1␤) was abolished. 7 It was also shown, by using bone marrow chimeras, that TLR4 expression on hematopoietic rather than parenchyma cells was instrumental in promoting liver IR-mediated damage. 8 TLR4 activation triggers 2 distinct signaling pathways leading to the induction of different immune-related genes. The MyD88...

show abstract

Section: Discussionmentioning

confidence: 99%

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Ultimately, myeloperoxidase (halide form, such as Cl -) released from neutrophils changes hydrogen peroxide (H2O2) into hypochlorous acid (HOCl), which is a potent oxidant. These oxidants can directly cause liver cell damage and/or induce protease-mediated injury through inactivation of the endogenous anti-protease system [15,16] , suggesting that anti-oxidant or anti-protease therapy would be helpful for preventing IRI.…”

Section: Kcs and Neutrophilsmentioning

confidence: 99%

Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide

Guan¹

2014

WJGS

152

133

View full text Add to dashboard Cite

Hepatic ischemia-reperfusion injury (IRI) is a pathophysiological event post liver surgery or transplantation and significantly influences the prognosis of liver function. The mechanisms of IRI remain unclear, and effective methods are lacking for the prevention and therapy of IRI. Several factors/pathways have been implicated in the hepatic IRI process, including anaerobic metabolism, mitochondria, oxidative stress, intracellular calcium overload, liver Kupffer cells and neutrophils, and cytokines and chemokines. The role of nitric oxide (NO) in protecting against liver IRI has recently been reported. NO has been found to attenuate liver IRI through various mechanisms including reducing hepatocellular apoptosis, decreasing oxidative stress and leukocyte adhesion, increasing microcirculatory flow, and enhancing mitochondrial function. The purpose of this review is to provide insights into the mechanisms of liver IRI, indicating the potential protective factors/pathways that may help to improve therapeutic regimens for controlling hepatic IRI during liver surgery, and the potential therapeutic role of NO in liver IRI.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Liver; Ischemia-reperfusion injury; Cytokine; Chemokine; Kupffer cells; Mitochondria; Nitric oxide Core tip: This review provides insights into several key mechanisms of liver ischemia-reperfusion injury, including the effects of anaerobic metabolism and the role of mitochondria, oxidative stress, intracellular calcium overload, liver Kupffer cells and neutrophils, and cytokines and chemokines; and summarizes the protective effects of nitric oxide.Guan LY, Fu PY, Li PD, Li ZN, Liu HY, Xin MG, Li W. Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide.

show abstract

“…One of us (C. W. S.) has recently reported on the molecules involved in the adherence of neutrophils to hepatocytes in vitro. In the absence of exogenous chemotactic activation, neutrophils adhered to cytokine-treated hepatocytes via LFA-1 and ICAM-1 [49]. Adhesion via activated Mac-1 is subsequently required for the release of proteolytic enzymes and reactive oxygen species by neutrophils that are cytotoxic to parenchymal cells in vitro (e.g., cardiac myocytes or hepatocytes).…”

Section: Comparison Of Homotypic and Heterotypic Adhesionmentioning

confidence: 99%

β2-Integrins mediate stable adhesion in collisional interactions between neutrophils and ICAM-1-expressing cells

Lynam

Sklar

Taylor

et al. 1998

Journal of Leukocyte Biology

View full text Add to dashboard Cite

The aggregation of human neutrophils in suspension has features that are analogous to their attachment to activated endothelium in that both involve selectin and ␤ 2 -integrin adhesion receptors. For the collisional interaction that forms neutrophil aggregates in suspension, there is a tethering step in which L-selectin on neutrophils binds PSGL-1. At relatively low shear rates (100-200 s -1 ) firm adhesion is mediated in equal measure by LFA-1 binding to ICAM-3, and Mac-1 binding to an as yet undefined ligand. In this report we used a mouse melanoma cell line expressing an estimated 700,000 ICAM-1 (CD54) to examine the relative roles of LFA-1 and Mac-1 over the kinetics of heterotypic cell adhesion in shear mixed suspensions. Neither heterotypic nor homotypic neutrophil aggregates formed with application of shear alone. However, the rate of aggregation peaked within seconds of chemotactic stimulation. In contrast to homotypic aggregation, neither L-selectin nor its O-glycoprotein ligands on neutrophils contributed to heterotypic adhesion. Adhesion was inhibited in a dose-dependent manner as ICAM-1 was titrated with blocking mAb. A direct interaction between LFA-1 and ICAM-1 was preferred over the first minute of stimulation, whereas at later times adhesion was supported equally by Mac-1. Activation with MnCl 2 also favored participation of the constitutively expressed LFA-1. Application of defined shear in a cone and plate viscometer showed that adhesion to the ICAM-1 cells decreased from a maximum level to baseline as shear rate increased up to 400 s -1 in a manner typical of integrin adhesion alone. In contrast, homotypic aggregation supported by the transition from selectin to integrin binding exhibited an increase in efficiency up to 800 s -1 . The pathophysiological significance of receptor site density and duration of contact in collisional interactions relevant to leukocyte recruitment compared to leukocyte-endothelial cell interactions on surfaces is discussed. J. Leukoc. Biol. 64: 622-630; 1998.

show abstract

CD18 integrin and CD54-dependent neutrophil adhesion to cytokine-stimulated human hepatocytes

Cited by 43 publications

References 0 publications

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion

Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide

β2-Integrins mediate stable adhesion in collisional interactions between neutrophils and ICAM-1-expressing cells

Contact Info

Product

Resources

About