Norberto Gonzalez-Juarbe is an associate professor working in the Infectious Diseases and Genomic Medicine Group. Currently, he is focused on 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 establish 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 on 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.
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
Tuberculosis (Edinburgh, Scotland). 2023-08-24; 102399.
Critical care (London, England). 2023-04-20; 27.1: 155.
PLoS pathogens. 2022-12-21; 18.12: e1011020.
A multiomics analysis of direct interkingdom dynamics between influenza A virus and Streptococcus pneumoniae uncovers host-independent changes to bacterial virulence fitness
Frontiers in microbiology. 2022-12-12; 13.946779.
PloS one. 2022-04-05; 17.4: e0265891.
mBio. 2022-02-22; 13.1: e0325721.
Pandemic Influenza Infection Promotes Streptococcus pneumoniae Infiltration, Necrotic Damage, and Proteomic Remodeling in the Heart
Journal of virology. 2021-09-27; 95.20: e0101021.
Cell reports. 2021-06-15; 35.11: 109267.
Streptococcus pneumoniae binds to host GAPDH on dying lung epithelial cells worsening secondary infection following influenza
mBio. 2021-05-04; 12.3:
Circulation research. 2021-03-05; 128.5: 570-584.
Molecular & cellular proteomics : MCP. 2020-12-01; 19.12: 2030-2047.
Cell reports. 2020-08-25; 32.8: 108062.
Cellular microbiology. 2020-01-01; 22.1: e13115.
Cell reports. 2018-07-10; 24.2: 429-440.
NAD+ Depletion Triggers Macrophage Necroptosis, a Cell Death Pathway Exploited by Mycobacterium tuberculosis
Scientific reports. 2018-04-11; 8.1: 5846.
Bacterial Pore-Forming Toxins Promote the Activation of Caspases in Parallel to Necroptosis to Enhance Alarmin Release and Inflammation During Pneumonia
American journal of respiratory and critical care medicine. 2017-09-01; 196.5: 609-620.
PLoS pathogens. 2017-08-25; 13.8: e1006582.
Streptococcus pneumoniae in the heart subvert the host response through biofilm-mediated resident macrophage killing
Cell death and differentiation. 2017-05-01; 24.5: 917-928.
Pore-forming toxin-mediated ion dysregulation leads to death receptor-independent necroptosis of lung epithelial cells during bacterial pneumonia
Annals of clinical microbiology and antimicrobials. 2017-03-29; 16.1: 19.
PloS one. 2017-02-16; 12.2: e0172314.
YopE specific CD8+ T cells provide protection against systemic and mucosal Yersinia pseudotuberculosis infection
PloS one. 2016-11-17; 11.11: e0166092.
Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases. 2016-09-01; 43.289-96.
CD8(+) T cells specific to a single Yersinia pseudotuberculosis epitope restrict bacterial replication in the liver but fail to provide sterilizing immunity
Infection and immunity. 2016-05-01; 84.5: 1457-69.
Infiltrated Macrophages Die of Pneumolysin-Mediated Necroptosis following Pneumococcal Myocardial Invasion
PLoS pathogens. 2015-12-11; 11.12: e1005337.
Infection and immunity. 2015-02-01; 83.2: 614-24.
mBio. 2013-10-15; 4.5: e00745-13.
Streptococcus pneumoniae biofilm formation is strain dependent, multifactorial, and associated with reduced invasiveness and immunoreactivity during colonization
This project utilizes genomics approaches to confirm the identity of the remains purported to be that of Leonardo da Vinci as well as to characterize the microbial population on aging artwork.