In vitro stimulation of neutrophil motility by metoprolol and sotalol related to inhibition of both H2O2 production and peroxidase mediated iodination of the cell and leucoattractant

Beta blockade in TBI: Dose-dependent reductions in BBB leukocyte mobilization and permeability in vivo

“…In vitro studies found that beta blockers enhance PMN motility in response to chemoattractants causing dose dependent inhibition of neutrophil CD11b expression, superoxide production and hydrogen peroxide release potentially explaining their observed decreased inflammation and foreshortened recovery time. [27][28][29] CD11b is a key surface PMN adhesion receptor believed to interact with endothelial counter receptors (ICAM-1, VCAM-1) and cause firm PMN-endothelial adhesion. 30 Polymorphonuclear neutrophil adhesion is preceded by rolling where the activated PMN interacts with activated endothelial cells mediated by Sialyl LewisX (sLeX) overexpression of surface endothelial receptors and surface PMN selectins, primarily L-selectin.…”

“…These data indicate beta blockade administration exerts an early and diffuse effect on interwoven elements essential for a coordinated immune response including hematopoietic progenitor elements. In vitro studies found that beta blockers enhance PMN motility in response to chemoattractants causing dose dependent inhibition of neutrophil CD11b expression, superoxide production and hydrogen peroxide release potentially explaining their observed decreased inflammation and foreshortened recovery time 27–29 . CD11b is a key surface PMN adhesion receptor believed to interact with endothelial counter receptors (ICAM-1, VCAM-1) and cause firm PMN-endothelial adhesion 30 .…”

Antiplatelet and Antileukocyte Effects of Cardiovascular,Immunomodulatory and Chemotherapeutic Drugs

“…MET and SOT caused significant stimulation of PMNL. Enhanced PMNL motility has been suggested to be related to -receptor blockade rather than to restricting the availability of hydrogen peroxide and reactive products of the MPO/H 2 O 2 /halide system [206].…”

Pathogenicity and virulence of black-pigmented Gram-negative anaerobes

“…The proteolytic activity of P. gingivalis only functions under anaerobic conditions, since the proteolytic enzymes of P. gingivalis are easily inactivated by H20 2 [63]. Only 6 × 10 -17 mol of H20 2 are required to inactivate the proteolytic activity of one cell, and this may be secreted by one activated polymorphonuclear leukocyte (PMN) [79,80]. As a virulence factor, the proteolytic activity of P. gingivalis may, therefore, only be fully expressed in tissue sites where an anaerobic environment has already been created.…”