Norberto Gonzalez-Juarbe, PhD

Assistant Professor

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

Publications

NAD+ Depletion Triggers Macrophage Necroptosis, a Cell Death Pathway Exploited by Mycobacterium tuberculosis.
Cell reports. 2018-07-10; 24.2: 429-440.
PMID: 29996103
Bacterial Pore-Forming Toxins Promote the Activation of Caspases in Parallel to Necroptosis to Enhance Alarmin Release and Inflammation During Pneumonia.
Scientific reports. 2018-04-11; 8.1: 5846.
PMID: 29643440
Severe Pneumococcal Pneumonia Causes Acute Cardiac Toxicity and Subsequent Cardiac Remodeling.
American journal of respiratory and critical care medicine. 2017-09-01; 196.5: 609-620.
PMID: 28614669
Streptococcus pneumoniae in the heart subvert the host response through biofilm-mediated resident macrophage killing.
PLoS pathogens. 2017-08-25; 13.8: e1006582.
PMID: 28841717
Pore-forming toxin-mediated ion dysregulation leads to death receptor-independent necroptosis of lung epithelial cells during bacterial pneumonia.
Cell death and differentiation. 2017-05-01; 24.5: 917-928.
PMID: 28387756
Killing of Serratia marcescens biofilms with chloramphenicol.
Annals of clinical microbiology and antimicrobials. 2017-03-29; 16.1: 19.
PMID: 28356113
YopE specific CD8+ T cells provide protection against systemic and mucosal Yersinia pseudotuberculosis infection.
PloS one. 2017-02-16; 12.2: e0172314.
PMID: 28207901
CD8(+) T cells specific to a single Yersinia pseudotuberculosis epitope restrict bacterial replication in the liver but fail to provide sterilizing immunity.
Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases. 2016-09-01; 43.289-96.
PMID: 27268148
Infiltrated Macrophages Die of Pneumolysin-Mediated Necroptosis following Pneumococcal Myocardial Invasion.
Infection and immunity. 2016-05-01; 84.5: 1457-69.
PMID: 26930705
Pore-Forming Toxins Induce Macrophage Necroptosis during Acute Bacterial Pneumonia.
PLoS pathogens. 2015-12-11; 11.12: e1005337.
PMID: 26659062
Requirement for Serratia marcescens cytolysin in a murine model of hemorrhagic pneumonia.
Infection and immunity. 2015-02-01; 83.2: 614-24.
PMID: 25422267
Streptococcus pneumoniae biofilm formation is strain dependent, multifactorial, and associated with reduced invasiveness and immunoreactivity during colonization.
mBio. 2013-10-15; 4.5: e00745-13.
PMID: 24129258

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