Research Opportunities Database

Joanna Szmydynger-Chodobska

Assistant Professor of Emergency Medicine (Research)

Department: Emergency Medicine

Phone: +1 401 444 8156

Email: Joanna_Szmydynger-Chodobska@Brown.EDU

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Location:

444-4285 - contact via e-mail - adam_chodobski@brown.edu or joanna_szmydynger-chodobska@brown.edu

Research Summary

Traumatic Brain Injury and Neuroinflammation Research involving the animal models of brain injury as well as clinical studies of patients with TBI have demonstrated that neurotrauma results in a rapid and substantial increase in CNS synthesis of proinflammatory cytokines, such as interleukin-1β and tumor necrosis factor-α. Shortly after the injury, there is a surge in production of proinflammatory cytokines in the injured brain parenchyma and their expression continues to be upregulated for several days after trauma. Proinflammatory cytokines not only promote an acute and delayed neuronal death, but can also interfere with survival signals generated by growth factors. In addition, proinflammatory cytokines exert various adverse effects on the BBB, including disruption of tight junctions and increase in the BBB permeability, the induction of expression of cell adhesion molecules, and production of chemokines. Although the role of proinflammatory cytokines in neuronal repair and long-term recovery is not completely understood, an early anti-inflammatory intervention has demonstrated beneficial effects in TBI. Dysfunction of the BBB observed after injury is central to the progression of post-traumatic neuroinflammation. Brain endothelium itself can be an important source of proinflammatory mediators, such as neutrophil and monocyte chemoattractants. Increased production of chemokines and augmented expression of cell adhesion molecules on the surface of cerebrovascular endothelium promote invasion of inflammatory cells with detrimental consequences to the integrity of neural tissue. Our laboratory has demonstrated that AVP contributes to dysfunction of the BBB by amplifying the synthesis of proinflammatory mediators and, consequently, promoting the invasion of inflammatory cells. However, the nature of these proinflammatory mediators and the signaling cascades involved are yet to be completely elucidated. We have also shown that AVP increases the loss of neural tissue occurring after injury, but it is currently unclear whether this phenomenon is related to AVP-mediated exacerbation of edema and inflammatory response or is associated with other AVP-dependent pathophysiological mechanisms. Our current investigations focus on answering these questions. If you would like to learn more about our research or become involved in our projects, please contact our office.

Past or Present Projects Available:

Project related to concussion and traumatic brain injury; involvement of blood-brain barrier and blood-CSF barrier; The Blood Brain Barriers and the Pathophysiology of a Traumatic Brain Injury