Among other research topics, Baruch Toledano is examining the immune system response to immune modulators. He is also interested in discovering the significant factors involved in adverse effects following cardiopulmonary bypass. The prevalence of congenital heart defects is 8 for every 1000 live births. Most of these children will need to undergo a cardiopulmonary bypass to repair this defect. Cardiopulmonary bypass, especially in children, is linked with significant inflammation, thus resulting in neutrophil activation and causing cellular lesions.
This exagerated inflammatory response can be observed in all newborns, while being present in only 5% of adults needing bypass surgery. The neutrophil seems to act as an essential mediator of tissue lesions associated with cardiopulmonary bypass and its related morbidity and mortality. Programmed cell death, or apoptosis, is a mechanism which controls the functional longevity of neutrophils found in tissues. Enhanced knowledge of modifications induced during neutrophil cell apoptosis, in addition to the eventual elimination of the inflammation effects brought on by this response, are crucial notions to the understanding of bypass tissue lesions.
Baruch Toledano and his team are working to answer questions regarding the newborn’s intrinsic susceptibility to display an aggravated inflammatory reaction responsible for the rise of morbidity and mortality rates associated with bypass surgery. With the appropriate patient modulations, it would be possible to force programmed neutrophil cellular death in order to avoid inflammatory response. This would result in reduced organ dysfunction symptoms and improved infant survival rates following bypass.
In addition, the team is studying the herpes simplex virus (HSV), the most frequent cause of sporadic viral encephalitis in North America. The host response to the herpes simplex virus is more frequently morbid or mortal in newborns than it is in adults. As of yet, there is no data to determine the infection effects of the herpes simplex virus 1 on apoptosis of neonatal neutrophilic cells.