scholarly journals Actin Is a Component of the Compensation Mechanism in Pseudorabies Virus Virions Lacking the Major Tegument Protein VP22

2005 ◽  
Vol 79 (13) ◽  
pp. 8614-8619 ◽  
Author(s):  
T. del Rio ◽  
C. J. DeCoste ◽  
L.W. Enquist
Keyword(s):  
Epithelial Cell ◽  
Cell Lines ◽  
Fusion Proteins ◽  
Pseudorabies Virus ◽  
Tegument Protein ◽  
Compensation Mechanism ◽  
Wild Type ◽  
Epithelial Cell Lines ◽  
Del Rio ◽  
Protein Vp22

ABSTRACT Despite being a major component of the pseudorabies virus tegument, VP22 is not required for PRV replication, virulence, or neuroinvasion (T. del Rio, H. C. Werner, and L. W. Enquist, J. Virol. 76:774-782, 2002). In the absence of VP22, tegument assembly compensates in a limited fashion with increased incorporation of cellular actin. Infection of epithelial cell lines expressing fluorescent actin fusion proteins resulted in the incorporation of filamentous and nonfilamentous actin into individual virions that were predominately light, noninfectious particles. We conclude that cellular actin is incorporated in the tegument of wild-type virions and is part of a compensation mechanism for VP22-null virions.

scholarly journals Infectious Epstein-Barr Virus Lacking Major Glycoprotein BLLF1 (gp350/220) Demonstrates the Existence of Additional Viral Ligands

2000 ◽  
Vol 74 (21) ◽  
pp. 10142-10152 ◽  
Author(s):  
Annette Janz ◽  
Muhsin Oezel ◽  
Christian Kurzeder ◽  
Josef Mautner ◽  
Dagmar Pich ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Lines ◽  
Epstein Barr Virus ◽  
Target Cells ◽  
Wild Type ◽  
Viral Glycoprotein ◽  
Barr Virus ◽  
Viral Mutant ◽  
Epithelial Cell Lines ◽  
Epstein Barr

ABSTRACT The binding of the viral major glycoprotein BLLF1 (gp350/220) to the CD21 cellular receptor is thought to play an essential role during infection of B lymphocytes by the Epstein-Barr virus (EBV). However, since CD21-negative cells have been reported to be infectible with EBV, additional interactions between viral and cellular molecules seem to be probable. Based on a recombinant genomic EBV plasmid, we deleted the gene that encodes the viral glycoprotein BLLF1. We tested the ability of the viral mutant to infect different lymphoid and epithelial cell lines. Primary human B cells, lymphoid cell lines, and nearly all of the epithelial cell lines that are susceptible to wild-type EBV infection could also be successfully infected with the viral mutant in vitro, although the efficiency of infection with BLLF1-negative virus was clearly lower than the one observed with wild-type EBV. Our studies show that the interaction between BLLF1 and CD21 is not absolutely required for the infection of lymphocytes and epithelial cells, indicating that viral molecules other than BLLF1 can mediate the binding of EBV to its target cells. In this context, our results further suggest the hypothesis that additional cellular molecules, apart from CD21, allow virus entry into these cells.

scholarly journals Pseudomonas aeruginosa Gene Products PilT and PilU Are Required for Cytotoxicity In Vitro and Virulence in a Mouse Model of Acute Pneumonia

1999 ◽  
Vol 67 (7) ◽  
pp. 3625-3630 ◽  
Author(s):  
James C. Comolli ◽  
Alan R. Hauser ◽  
Leslie Waite ◽  
Cynthia B. Whitchurch ◽  
John S. Mattick ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cell ◽  
Mouse Model ◽  
Cell Lines ◽  
Twitching Motility ◽  
Wild Type ◽  
Epithelial Cell Lines ◽  
Acute Pneumonia

ABSTRACT Type IV pili of the opportunistic pathogen Pseudomonas aeruginosa mediate twitching motility and act as receptors for bacteriophage infection. They are also important bacterial adhesins, and nonpiliated mutants of P. aeruginosa have been shown to cause less epithelial cell damage in vitro and have decreased virulence in animal models. This finding raises the question as to whether the reduction in cytotoxicity and virulence of nonpiliated P. aeruginosa mutants are primarily due to defects in cell adhesion or loss of twitching motility, or both. This work describes the role of PilT and PilU, putative nucleotide-binding proteins involved in pili function, in mediating epithelial cell injury in vitro and virulence in vivo. Mutants of pilT and pilU retain surface pili but have lost twitching motility. In three different epithelial cell lines, pilT or pilU mutants of the strain PAK caused less cytotoxicity than the wild-type strain but more than isogenic, nonpiliated pilA or rpoN mutants. ThepilT and pilU mutants also showed reduced association with these same epithelial cell lines compared both to the wild type, and surprisingly, to a pilA mutant. In a mouse model of acute pneumonia, the pilT and pilUmutants showed decreased colonization of the liver but not of the lung relative to the parental strain, though they exhibited no change in the ability to cause mortality. These results demonstrate that pilus function mediated by PilT and PilU is required for in vitro adherence and cytotoxicity toward epithelial cells and is important in virulence in vivo.

scholarly journals Essential Role of Visfatin in Lipopolysaccharide and Colon Ascendens Stent Peritonitis-Induced Acute Lung Injury

2019 ◽  
Vol 20 (7) ◽  
pp. 1678 ◽  
Author(s):  
Yi-Chen Lee ◽  
Chun-Yu Lin ◽  
Yen-Hsu Chen ◽  
Wen-Chin Chiu ◽  
Yen-Yun Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Epithelial Cell ◽  
Lung Injury ◽  
Cell Lines ◽  
Inflammatory Cytokines ◽  
Bronchial Epithelial Cell ◽  
Bronchial Epithelial ◽  
Epithelial Cell Lines ◽  
Nfκb Pathway ◽  
Pro Inflammatory Cytokines

Acute lung injury (ALI) is a life-threatening syndrome characterized by acute and severe hypoxemic respiratory failure. Visfatin, which is known as an obesity-related cytokine with pro-inflammatory activities, plays a role in regulation of inflammatory cytokines. The mechanisms of ALI remain unclear in critically ill patients. Survival in ALI patients appear to be influenced by the stress generated by mechanical ventilation and by ALI-associated factors that initiate the inflammatory response. The objective for this study was to understand the mechanisms of how visfatin regulates inflammatory cytokines and promotes ALI. The expression of visfatin was evaluated in ALI patients and mouse sepsis models. Moreover, the underlying mechanisms were investigated using human bronchial epithelial cell lines, BEAS-2B and NL-20. An increase of serum visfatin was discovered in ALI patients compared to normal controls. Results from hematoxylin and eosin (H&E) and immunohistochemistry staining also showed that visfatin protein was upregulated in mouse sepsis models. Moreover, lipopolysaccharide (LPS) induced visfatin expression, activated the STAT3/NFκB pathway, and increased the expression of pro-inflammatory cytokines, including IL1-β, IL-6, and TNF-α in human bronchial epithelial cell lines NL-20 and BEAS-2B. Co-treatment of visfatin inhibitor FK866 reversed the activation of the STAT3/NFκB pathway and the increase of pro-inflammatory cytokines induced by LPS. Our study provides new evidence for the involvement of visfatin and down-stream events in acute lung injury. Further studies are required to confirm whether the anti-visfatin approaches can improve ALI patient survival by alleviating the pro-inflammatory process.

Expressional pattern of chaperones in neuronal, glial, amnion, mesothelial, and bronchial epithelial cell lines

2003 ◽  
Vol 80 (4) ◽  
pp. 444-450 ◽  
Author(s):  
Jae-Kyung Myung ◽  
Kurt Krapfenbauer ◽  
Rachel Weitzdoerfer ◽  
Andreas Peyrl ◽  
Michael Fountoulakis ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Lines ◽  
Bronchial Epithelial Cell ◽  
Bronchial Epithelial ◽  
Epithelial Cell Lines

scholarly journals Expression of junctional proteins in choroid plexus epithelial cell lines: a comparative study

2007 ◽  
Vol 4 (1) ◽  
pp. 11 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Crissey L Pascale ◽  
Andrew N Pfeffer ◽  
Cassaundra Coulter ◽  
Adam Chodobski
Keyword(s):  
Epithelial Cell ◽  
Comparative Study ◽  
Choroid Plexus ◽  
Cell Lines ◽  
Choroid Plexus Epithelial Cell ◽  
Junctional Proteins ◽  
Epithelial Cell Lines ◽  
Choroid Plexus Epithelial
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