Brenda Laster
Researcher
Address:
Brenda Laster
Ben Gurion University
Department of Nuclear Engineering
POB 653
84105 Beer Sheva
IsraelPhone number:
(972) 8-647-9636
Fax Number:
(072)233-1497
Suggestions for potential research cooperations:
I am looking for collaborators who would like to examine whether hydrogen peroxide (H2O2) can be used to control inflammation. Depending upon the number of infectious particles and their replication rate, cell receptors are up-regulated, chemokines and pro-inflammatory cytokines are released by the affected cells, and neutrophils are recruited to the regions of damage. Their secretion of H2O2 and superoxide (upon its conversion to H2O2 by superoxide dismutase enzymes (SODs), increases the level of oxidative damage in the region through protein oxidation and lipid peroxidation. This additional oxidative damage can result in a vicious and self-repetitive cycle of damage detection and inflammatory response. The question is raised whether the damage produced by H2O2 can potentially induce an adaptive immune response to the oxidative molecular patterns (damage-associated molecular patterns).
The multiple roles of H2O2 in inflammation have been reported. At H2O2 concentrations that are typical of a normal inflammatory condition, when simultaneously present with TNF-α, act synergistically to increase the severity of inflammation. Conversely, the same concentration of H2O2, without TNF-α, modulates inflammation by inducing expression of the heme oxygenase gene and its antioxidant by-products, CO and bilirubin.
More importantly, the role of H2O2 in cell signaling indirectly affects whether pro- or anti-inflammatory cytokines are secreted by the cell. This is a consequence of its reversible oxidation of cysteines in the catalytic core of phosphatase enzymes, such as MKP-1 and its inactivation of these phosphatases. Because cell signaling is regulated by protein phosphorylation and dephosphorylation, the inactivation of phosphatases by H2O2, in a concentration-dependent manner, prolongs or curtails the activation of particular molecules in the NF-κB and MAPK oxidative stress pathways.
Additionally, sulfenic acid is a by-product of cysteine oxidation by H2O2. The reversible activation of sulfenic acid is also reported to be a requirement for the activation and function of naïve T and B cells.
The ingestion of low, non-toxic concentrations of H2O2 has been recommended by alternative vast variety of inflammatory diseases. In this community, the reasons for the success of the treatment have never been medicine physicians for over 100 years as a treatment for a explained. Subsequent scientific and technological advances have now made it possible to examine its role in inflammation. If the DAMPs produced by H2O2 are recognized by T and B cells of the adaptive immune system, it might be possible to use this molecule to control the level of inflammation induced by infectious pathogens. In addition to preventing sepsis, this approach might prevent the progress of an acute inflammatory condition to that of chronic inflammation which is associated with cancer development.
I am looking for collaborators who would like to examine whether hydrogen peroxide (H2O2) can be used to control inflammation. Depending upon the number of infectious particles and their replication rate, cell receptors are up-regulated, chemokines and pro-inflammatory cytokines are released by the affected cells, and neutrophils are recruited to the regions of damage. Their secretion of H2O2 and superoxide (upon its conversion to H2O2 by superoxide dismutase enzymes (SODs), increases the level of oxidative damage in the region through protein oxidation and lipid peroxidation. This additional oxidative damage can result in a vicious and self-repetitive cycle of damage detection and inflammatory response. The question is raised whether the damage produced by H2O2 can potentially induce an adaptive immune response to the oxidative molecular patterns (damage-associated molecular patterns).
The multiple roles of H2O2 in inflammation have been reported. At H2O2 concentrations that are typical of a normal inflammatory condition, when simultaneously present with TNF-α, act synergistically to increase the severity of inflammation. Conversely, the same concentration of H2O2, without TNF-α, modulates inflammation by inducing expression of the heme oxygenase gene and its antioxidant by-products, CO and bilirubin.
More importantly, the role of H2O2 in cell signaling indirectly affects whether pro- or anti-inflammatory cytokines are secreted by the cell. This is a consequence of its reversible oxidation of cysteines in the catalytic core of phosphatase enzymes, such as MKP-1 and its inactivation of these phosphatases. Because cell signaling is regulated by protein phosphorylation and dephosphorylation, the inactivation of phosphatases by H2O2, in a concentration-dependent manner, prolongs or curtails the activation of particular molecules in the NF-κB and MAPK oxidative stress pathways.
Additionally, sulfenic acid is a by-product of cysteine oxidation by H2O2. The reversible activation of sulfenic acid is also reported to be a requirement for the activation and function of naïve T and B cells.
The ingestion of low, non-toxic concentrations of H2O2 has been recommended by alternative vast variety of inflammatory diseases. In this community, the reasons for the success of the treatment have never been medicine physicians for over 100 years as a treatment for a explained. Subsequent scientific and technological advances have now made it possible to examine its role in inflammation. If the DAMPs produced by H2O2 are recognized by T and B cells of the adaptive immune system, it might be possible to use this molecule to control the level of inflammation induced by infectious pathogens. In addition to preventing sepsis, this approach might prevent the progress of an acute inflammatory condition to that of chronic inflammation which is associated with cancer development.
Your research topics:
antimicrobial resistance
prevention
treatment
Special methods/technologies:
Molecular Biology
