4 results match your criteria: "Soroka Medical University Center and Ben-Gurion University of the Negev[Affiliation]"
Pharmacological preconditioning with adenosine A(1) receptor agonist suppresses cellular immune response by an A(2A) receptor dependent mechanism.
Int Immunopharmacol
May 2014
Department of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O.B. 653, Beer-Sheva 84105, Israel.
Under stressful conditions such as ischemia, sepsis, and severe trauma, adenosine levels are elevated and protect the tissue by interaction with G coupled receptors. In a model of peritonitis, we previously found that pharmacological preconditioning (PPC) of mice with a selective adenosine A1 receptor (A1R) agonist, 2-chloro-N(6)-cyclopentyladenosine (CCPA), induced the A2AR which reduces cytokine secretion and leukocyte recruitment. In our present study we determined whether mice PPC will moderate cellular immune response by the same mechanism.
View Article and Find Full Text PDFEndothelial ICAM-1 protein induction is regulated by cytosolic phospholipase A2α via both NF-κB and CREB transcription factors.
J Immunol
February 2011
Infectious Disease and Immunology Laboratory, Clinical Biochemistry Department, Faculty of Health Sciences, Soroka Medical University Center and Ben-Gurion University of the Negev, Beer Sheva 84105, Israel.
Article Synopsis
- The study investigates the role of cPLA(2)α in the overexpression of ICAM-1 during inflammation, highlighting its importance in immune responses.
- cPLA(2)α and ICAM-1 were found to be elevated in inflamed tissues of mice, and reducing cPLA(2)α levels led to decreased ICAM-1 overexpression, indicating a significant relationship between the two.
- The research also reveals that cPLA(2)α activation involves upstream signals from NADPH oxidase and is necessary for subsequent events like NF-κB and CREB phosphorylation, which are crucial for ICAM-1 upregulation.
Regulation of adenosine system at the onset of peritonitis.
Nephrol Dial Transplant
March 2010
Department of Clinical Biochemistry, Soroka Medical University Center and Ben-Gurion University of the Negev, Beer-Sheva 84101, Israel.
Background: Adenosine, a potent regulator of inflammation, is produced under stressful conditions due to degradation of ATP/ADP by the ectoenzymes CD39 and CD73. Adenosine is rapidly degraded by adenosine deaminase (ADA) or phosphorylated in the cell by adenosine kinase (AK). From four known receptors to adenosine, A(1) (A(1)R) promotes inflammation by a G(i)-coupled receptor.
View Article and Find Full Text PDFAnti-inflammatory preconditioning by agonists of adenosine A1 receptor.
PLoS One
May 2008
Department of Clinical Biochemistry, Soroka Medical University Center and Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Background: Adenosine levels rise during inflammation and modulate inflammatory responses by engaging with four different G protein-coupled receptors. It is suggested that adenosine exhibits pro-inflammatory effects through its A(1) receptor (A(1)R), and anti-inflammatory effects through A(2A) receptor (A(2A)R). Therefore, understanding of the mechanisms that govern adenosine receptor regulation may advance treatment of various inflammatory disorders.
View Article and Find Full Text PDF