scholarly journals A Functional IFN-γ-Inducible Protein-10/CXCL10-Specific Receptor Expressed by Epithelial and Endothelial Cells That Is Neither CXCR3 Nor Glycosaminoglycan

2001 ◽  
Vol 167 (11) ◽  
pp. 6576-6582 ◽  
Author(s):  
Kenzo Soejima ◽  
Barrett J. Rollins
Keyword(s):  
Endothelial Cells ◽  
Specific Receptor ◽  
Ifn Γ ◽  
Inducible Protein

CD40 amplifies Fas-mediated apoptosis: a mechanism contributing to emphysema

2012 ◽  
Vol 303 (2) ◽  
pp. L141-L151 ◽  
Author(s):  
Ayako Shigeta ◽  
Yuji Tada ◽  
Ji-Yang Wang ◽  
Shunsuke Ishizaki ◽  
Junichi Tsuyusaki ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Pulmonary Emphysema ◽  
Alveolar Epithelial Cells ◽  
Alveolar Cells ◽  
Alveolar Epithelial ◽  
Cd40 Stimulation ◽  
Ifn Γ ◽  
Apoptosis And Inflammation

Excessive apoptosis and prolonged inflammation of alveolar cells are associated with the pathogenesis of pulmonary emphysema. We aimed to determine whether CD40 affects alveolar epithelial cells and endothelial cells, with regard to evoking apoptosis and inflammation. Mice were repeatedly treated with agonistic-anti CD40 antibody (Ab), with or without agonistic-anti Fas Ab, and evaluated for apoptosis and inflammation in lungs. Human pulmonary microvascular endothelial cells and alveolar epithelial cells were treated with agonistic anti-CD40 Ab and/or anti-Fas Ab to see their direct effect on apoptosis and secretion of proinflammatory molecules in vitro. Furthermore, plasma soluble CD40 ligand (sCD40L) level was evaluated in patients with chronic obstructive pulmonary disease (COPD). In mice, inhaling agonistic anti-CD40 Ab induced moderate alveolar enlargement. CD40 stimulation, in combination with anti-Fas Ab, induced significant emphysematous changes and increased alveolar cell apoptosis. CD40 stimulation also enhanced IFN-γ-mediated emphysematous changes, not via apoptosis induction, but via inflammation with lymphocyte accumulation. In vitro, Fas-mediated apoptosis was enhanced by CD40 stimulation and IFN-γ in endothelial cells and by CD40 stimulation in epithelial cells. CD40 stimulation induced secretion of CCR5 ligands in endothelial cells, enhanced with IFN-γ. Plasma sCD40L levels were significantly increased in patients with COPD, inversely correlating to the percentage of forced expiratory volume in 1 s and positively correlating to low attenuation area score by CT scan, regardless of smoking history. Collectively CD40 plays a contributing role in the development of pulmonary emphysema by sensitizing Fas-mediated apoptosis in alveolar cells and increasing the secretion of proinflammatory chemokines.

scholarly journals Gamma Interferon Mediates Experimental Cerebral Malaria by Signaling within Both the Hematopoietic and Nonhematopoietic Compartments

2017 ◽  
Vol 85 (11) ◽  
Author(s):  
Ana Villegas-Mendez ◽  
Patrick Strangward ◽  
Tovah N. Shaw ◽  
Ivana Rajkovic ◽  
Vinko Tosevski ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cerebral Malaria ◽  
Myeloid Cell ◽  
Gamma Interferon ◽  
Cell Populations ◽  
Experimental Cerebral Malaria ◽  
Cerebral Pathology ◽  
Multiple Cell ◽  
Ifn Γ

ABSTRACT Experimental cerebral malaria (ECM) is a gamma interferon (IFN-γ)-dependent syndrome. However, whether IFN-γ promotes ECM through direct and synergistic targeting of multiple cell populations or by acting primarily on a specific responsive cell type is currently unknown. Here, using a panel of cell- and compartment-specific IFN-γ receptor 2 (IFN-γR2)-deficient mice, we show that IFN-γ causes ECM by signaling within both the hematopoietic and nonhematopoietic compartments. Mechanistically, hematopoietic and nonhematopoietic compartment-specific IFN-γR signaling exerts additive effects in orchestrating intracerebral inflammation, leading to the development of ECM. Surprisingly, mice with specific deletion of IFN-γR2 expression on myeloid cells, T cells, or neurons were completely susceptible to terminal ECM. Utilizing a reductionist in vitro system, we show that synergistic IFN-γ and tumor necrosis factor (TNF) stimulation promotes strong activation of brain blood vessel endothelial cells. Combined, our data show that within the hematopoietic compartment, IFN-γ causes ECM by acting redundantly or by targeting non-T cell or non-myeloid cell populations. Within the nonhematopoietic compartment, brain endothelial cells, but not neurons, may be the major target of IFN-γ leading to ECM development. Collectively, our data provide information on how IFN-γ mediates the development of cerebral pathology during malaria infection.

Salvianolic acid B suppresses IFN-γ-induced JAK/STAT1 activation in endothelial cells

2011 ◽  
Vol 128 (6) ◽  
pp. 560-564 ◽  
Author(s):  
Shih Chung Chen ◽  
Yun Lian Lin ◽  
Bin Huang ◽  
Danny Ling Wang ◽  
Jing Jy Cheng
Keyword(s):  
Endothelial Cells ◽  
Salvianolic Acid B ◽  
Salvianolic Acid ◽  
Ifn Γ

scholarly journals Human genetic deficiencies reveal the roles of complement in the inflammatory network: Lessons from nature

2009 ◽  
Vol 106 (37) ◽  
pp. 15861-15866 ◽  
Author(s):  
Knut Tore Lappegård ◽  
Dorte Christiansen ◽  
Anne Pharo ◽  
Ebbe Billmann Thorgersen ◽  
Bernt Christian Hellerud ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Gram Negative Bacteria ◽  
Enzyme Release ◽  
Experimental Conditions ◽  
Gram Negative ◽  
Cytokines And Chemokines ◽  
Ifn Γ ◽  
Inducible Protein ◽  
The Complement System

Complement component C5 is crucial for experimental animal inflammatory tissue damage; however, its involvement in human inflammation is incompletely understood. The responses to Gram-negative bacteria were here studied taking advantage of human genetic complement-deficiencies—nature's own knockouts—including a previously undescribed C5 defect. Such deficiencies provide a unique tool for investigating the biological role of proteins. The experimental conditions allowed cross-talk between the different inflammatory pathways using a whole blood model based on the anticoagulant lepirudin, which does not interfere with the complement system. Expression of tissue factor, cell adhesion molecules, and oxidative burst depended highly on C5, mediated through the activation product C5a, whereas granulocyte enzyme release relied mainly on C3 and was C5a-independent. Release of cytokines and chemokines was mediated to varying degrees by complement and CD14; for example, interleukin (IL)-1β and IL-8 were more dependent on complement than IFN-γ and IL-6, which were highly dependent on CD14. IL-1 receptor antagonist (IL-1ra) and IFN-γ inducible protein 10 (IP-10) were fully dependent on CD14 and inversely regulated by complement, that is, complement deficiency and complement inhibition enhanced their release. Granulocyte responses were mainly complement-dependent, whereas monocyte responses were more dependent on CD14. Notably, all responses were abolished by combined neutralization of complement and CD14. The present study provides important insight into the comprehensive role of complement in human inflammatory responses to Gram-negative bacteria.

scholarly journals TNF-α, IL-4, and IFN-γ Regulate Differential Expression of P- and E-Selectin Expression by Porcine Aortic Endothelial Cells

2000 ◽  
Vol 164 (6) ◽  
pp. 3309-3315 ◽  
Author(s):  
Claire J. Stocker ◽  
Katharine L. Sugars ◽  
Olivier A. Harari ◽  
R. Clive Landis ◽  
Bernard J. Morley ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Differential Expression ◽  
Aortic Endothelial Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Porcine Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Targeting the Function of IFN-γ-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis

2002 ◽  
Vol 169 (5) ◽  
pp. 2685-2693 ◽  
Author(s):  
Izhar Salomon ◽  
Nir Netzer ◽  
Gizi Wildbaum ◽  
Sagie Schif-Zuck ◽  
Gila Maor ◽  
...  
Keyword(s):  
Adjuvant Arthritis ◽  
Ifn Γ ◽  
Inducible Protein

Vibrio parahaemolyticus elevates interferon alpha production in intestinal-like epithelial Caco-2 cells

2007 ◽  
Vol 53 (9) ◽  
pp. 1084-1090
Author(s):  
Xin Lian ◽  
Akira Takahashi ◽  
Masayuki Nakano ◽  
Emiko Hori ◽  
Kazuaki Mawatari ◽  
...  
Keyword(s):  
Interferon Alpha ◽  
Vibrio Parahaemolyticus ◽  
Intestinal Loop ◽  
Gene Expressions ◽  
Tetratricopeptide Repeats ◽  
Mucosal Cells ◽  
Ifn Γ ◽  
Polymerase Chain ◽  
Inducible Protein ◽  
Gene Expression Levels

Vibrio parahaemolyticus is the leading cause of gastroenteritis from seafood consumption. We tried to determine how the gene expression levels of intestinal-like epithelial cells (Caco-2 cells) and mouse intestinal loop mucosal cells change upon infection with this bacterium. Since we found the robust production of interferon alpha (IFN-α) by the V. parahaemolyticus infection, we also assessed the upregulation of a number of IFN-stimulated genes (ISGs). The expressions of IFN protein were determined by Western blotting, and the gene expressions of Caco-2 cells after V. parahaemolyticus infection were determined by quantitative real-time reverse-transcription polymerase chain reaction. Three ISGs (i.e., IFN-α-inducible protein 15, IFN-α-inducible protein 6-16, and IFN-induced protein with tetratricopeptide repeats 1) were upregulated by V. parahaemolyticus infection. Infection induced the production of IFN-α, but not IFN-β or IFN-γ. The upregulation of the 3 ISGs was suppressed by treatment with a neutralizing IFN-α antibody. Moreover, the production of infection-induced IFN-α was found in the mouse intestinal loop mucosal cells. V. parahaemolyticus infection of Caco-2 cells results in IFN-α production and the expression of IFN-regulated genes.

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