SEMINARS

  

FALL SEMINAR SERIES                       

Comparative Biomedical Sciences                  

School of Veterinary Medicine

Room 1212C - 12 Noon

 


 

December 7, 2017

 

Tomislav Jelesijevic, DVM, PhD, DACVP

Senior Research Associate

Department of Infectious Diseases

University of Georgia Athens

 

Host: Dr. Michael Mathis

 

“Challenges in Developing Highly Effective Treatments and Vaccine for Glanders”

 

Burkholderia mallei is a Gram- negative bacterium that causes a life-threatening zoonotic disease glanders. The disease is endemic in soliped populations of Asia, Africa, the Middle East and South America. Due to high mortality, history of use as a bioweapon, lack of vaccines, and paucity of antibiotic treatment options, B. mallei is classified as a Tier 1 Select Agent and developing countermeasures is a priority. The pathogenesis of glanders is complex and involves the extracellular/intracellular replication of B. mallei and dissemination to target tissues (lungs, spleen, liver, lymph nodes) where it forms chronic lesions that are difficult to treat. Efforts during the last decade to develop glanders vaccines have yielded a range of candidates including inactivated bacteria, subunit vaccines, and live attenuated strains (LAS). So far LAS provide the best protection in acute lethal infection studies, but fail to provide sterile immunity. Survivors develop pyogranulomatous lesions in target tissues and ultimately succumb to chronic infection. Efforts to understand mechanism of persistent infection have led to our discovery that myeloid-derived suppressor cells (MDSCs) are present in target organs of chronically-infected mice. Preliminary data also demonstrate a direct correlation between the extent of bacterial burden in tissues and the relative numbers of MDSCs. Given their ability to suppress innate and adaptive immune responses, we propose that MDSCs accumulate in target organs of mice surviving acute lethal infection and suppress the immune response against B. mallei. This, in turn, may preclude elimination of the infection and result in the development of hallmark chronic glanders lesions.

 

 

December 14, 2017

 

Jyokita Sharma, PhD

Associate Professor

Department of Biomedical Sciences

School of Medicine & Health Sciences

University of North Dakota

 

Host: Dr. Yogesh Saini

 

“Neutrophil Extracellular Traps: Formation and Therapeutic Implications”

 

Major focus of Sharma lab is Host-pathogen interaction, role of C-type lectin receptors and neutrophil function in regulation of inflammation in bacterial pneumonia, sepsis, CGD (chronic granulomatous disease) and cigarette smoke exacerbation of COPD (Chronic Obstructive pulmonary Diseases). For our hypothesis driven research we work extensively with transgenic mouse strains as preclinical disease models as well as patient samples that we obtain through our collaborations with clinicians at the National Institutes of Health, Altru Clinic and the Department of Surgery at UND. The lab has a number of ongoing projects, one of which is elucidation of molecular mechanisms of neutrophil extracellular trap formation. Neutrophils are the first responders for combating microbial infection. The traditional antimicrobial program of neutrophils mainly constitutes phagocytosis followed by production of noxious agents such as reactive oxygen species (ROS) to kill internalized microbes. A novel paradigm in neutrophil antimicrobial program, however, is the formation of extracellular traps (Neutrophil Extracellular Traps, NETs), which are DNA fibrils expelled by these cells that are decorated with granular contents such as various proteases. NETs have been reported to play protective roles in infectious diseases by trapping, neutralizing and killing extracellular microbes. On the flip side, an exuberant NET formation has been linked to development of many inflammatory diseases or disorders by promoting hyper activated immune response. This indicates that NET formation needs to be tightly regulated and fine-tuned in a microenvironment dependent manner. To harness the beneficial outcome of NETs while avoiding their potentially harmful effects, a clear understanding of the molecular mechanism of neutrophil NET formation is essential. 

 

Thanks to our Guest Speakers for Fall 2017

 

Thursday, August 31, 2017

Thank you, Dr. Min Wu!

Professor of Immunology & Microbiology
Department of Biochemistry and Molecular Biology
University of North Dakota

 

Thursday, September 28, 2017

Thank you, Dr. Isabelle Miousse!

Postdoctoral Fellow
Department of Environmental and Occupational Health
University of Arkansas for Medical Sciences

 

Thursday, October 12, 2017

Thank you, Dr. Hongju Wu!

Associate Professor
Departments of Medicine and Physiology
Tulane University School of Medicine, New Orleans

 

Thursday, October 19, 2017

Thank you, Dr. Lung-Chi Chen!

Professor of Environmental Medicine
Department of Environmental Medicine
New York University School of Medicine

 

Thursday, October 26, 2017

Thank you, Dr. Enid Neptune!

Associate Professor of Medicine
Division of Pulmonary and Critical Care Medicine
Department of Medicine, John Hopkins University

 

Thursday, November 16, 2017

Thank you, Dr. Jacob Raber!

Professor
Behavioral Neuroscience, Neurology and Radiation Medicine
Oregon Health & Science University

 

Thursday, November 16, 2017

Thank you, Dr. Kent Pinkerton!

Director and Deputy Director
Center for Health and Environment, Western Center for Agricultural Health and Safety, and Environmental Health Science Core Center
University of California, Davis

 

 

JOURNAL CLUB - FALL 2017

Room 2502 - School of Veterinary Medicine

Tuesday, December 12, 2017

12 Noon

 

"Mincle-Mediated Neutrophil Extracellular Trap Formation by Regulation of Autophagy"

 

An article from the lab of Dr. Jyotika Sharma, the CBS guest speaker for December 14, 2017

Presented by Brandon Lewis