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Dr. De Rivero Vaccari






Research Interests


Curriculum Vitae




 Contact Information:

The Miami Project to
Cure Paralysis

1095 NW 14th Terrace

Locator Code R-48

Miami, Florida 33136

Tel:  (305) 243-7113


Home > Our Research Faculty > Juan Pablo De Rivero Vaccari, Ph.D.



Research Assistant Professor, Department of Neurological Surgery



Underlying mechanisms of the innate immune response and contributions to various CNS diseases.


Research Interests

My research focuses on understanding early inflammatory events in central nervous system (CNS) trauma. Currently, my laboratory is focusing on the effects of pattern recognition receptor (PRR)-activation after spinal cord injury (SCI) and stroke.

The immune response is divided into two phases: Innate immunity and adaptive immunity. The innate immune phase corresponds to the early events of the inflammatory response and precedes the adaptive immune phase.  It is classically defined as the first line of defense against infections or damage. It is initiated by danger-associated molecular patterns (DAMPs) or by pathogen-associated molecular patterns (PAMPs) that are recognized by pattern recognition receptors (PRRs). DAMPs are endogenous ligands such as ATP, DNA or RNA, whereas PAMPs include exogenous activators like bacterial lipopolysaccharide or bacterial flagellin.

In addition, we study biomarkers as therapeutic and diagnostic options that can be eventually used as therapeutic targets to improve outcomes after CNS injury and disease. The development of biomarkers for CNS injury and disease will be useful to determine the severity of damage to the CNS as well as the recovery potential. The predictive value of biomarkers early in SCI pathology is relevant in choosing a particular neuroprotective treatment in the acute phase. Therefore, an early, accurate diagnostic test designed to target neuroprotective strategies is a desirable prognostic tool.

Of particular interest to us is the role of the inflammasome, a multiprotein complex involved in the activation of caspase-1 and the processing of the pro-inflammatory cytokines IL-1 and IL-18, after CNS injury. We have previously shown that the inflammasome is activated after spinal cord injury (de Rivero Vaccari et al. J Neurosci 2008) and brain injury (de Rivero Vaccari et al. J Cerebral Blood Flow and Metabolism 2009). Accordingly, we have shown that the inflammasome can be inhibited in order to improve histopathological and functional outcomes after CNS injury by decreasing the inflammatory response.


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