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Norberto Gonzalez-Juarbe is an assistant professor working in the Infectious Diseases and Genomic Medicine Group. Currently, he is focused in the host responses that occur during co- and secondary bacterial infections to influenza.
Dr. Gonzalez-Juarbe began his science career researching the habitability of primary producers in the field of astrobiology. Later while working on his PhD, his research was one of the first to established that bacterial pathogens use pore-forming toxins to deplete the lungs of alveolar macrophages through activation of necroptosis (programmed necrosis).
As a postdoctoral fellow at the University of Alabama in Birmingham, under the supervision of Dr. Carlos Orihuela, Dr. Gonzalez-Juarbe focused in the study of Streptococcus pneumoniae-induced cardiac damage during invasive pneumococcal disease and expanded his graduate work on how bacterial pore-forming toxins cause cell death and the immunological implications of these mechanisms.
Dr. Gonzalez-Juarbe earned his BS in microbiology from the University of Puerto Rico at Arecibo and his PhD in microbiology and immunology at the University of Texas Health–San Antonio under the supervision of Dr. Molly A. Bergman.
Research Priorities
Understanding the role of programmed necrosis during secondary bacterial infections to influenza
- Influenza infection promotes an extremely severe form of secondary bacterial pneumonia, characterized by necrotic lung damage and significantly increased mortality. We aim to identify the molecular mechanisms behind this synergism.
- Emphasis in the role of ion dysregulation
- Understanding the role of oxidative stress in the potentiation of necroptosis
Understanding the role of influenza infection in cardiac damage
- We aim to discern the effects of influenza infection in the modulation of cardiomyocyte death and its effect during secondary bacterial infections
- Discern the effect of influenza infection in bacterial adhesion molecules in the myocardium.
Understanding the role of programmed cell death pathways in the release of damage-associated molecular patterns during secondary bacterial infections to influenza
- Integration of multiple omics technologies
- Mechanism of how influenza initiated cellular mechanism affect bacterial induced inflammation