Jian-Dong Li, M.D., Ph.D.
Inflammation and Immunity
Georgia State University

Research Interests

Inflammation is a hallmark of many serious human inflammatory diseases including infectious diseases, chronic obstructive pulmonary diseases, otitis media, asthma, arthritis, inflammatory bowel disease, atherosclerosis and cancer. We primarily focus on understanding the molecular basis of inflammatory diseases and further developing novel anti-inflammatory therapeutic agents.

Research Vision

Appropriate inflammation is a protective host defense response to remove the injurious stimuli as well as initiate tissue healing and the repair process. However, overactive inflammation is detrimental to the host, leading to inflammatory diseases. Thus, inflammation must be tightly regulated. In contrast to the positive regulation, inducible negative feedback regulation plays an important role in preventing overactive inflammation. Understanding the molecular mechanisms underlying tight regulation of inflammation will lead to development of novel anti-inflammatory strategies. Moreover, because inflammation is a complex biological response of the body to harmful stimuli, interdisciplinary collaborative efforts would be critical for fully understanding the molecular pathogenesis and thus accelerating the successful development of novel therapeutics.

In the Lab

In my laboratory, multidisciplinary approaches have been undertaken. Those approaches include molecular genetics, cell biology, biochemistry, molecular biology, immunology, chemical biology, pharmacology, functional genomics and proteomics as well as transgenic animals. Currently, we are focusing on the following research areas:

Inducible Negative Feedback Regulation of Inflammation.We recently found that CYLD, a deubiquitinase, acts as an inducible negative feedback regulator for inflammation. Our studies provide novel insights into the tight regulation of inflammation and may lead to the identification of novel therapeutic targets. Our future studies will focus on identifying the novel molecular targets of CYLD and the underlying signaling mechanisms involved in inflammatory and infectious diseases. We will also investigate the mechanisms by which CYLD is induced.

Regulation of Host Survival in S. pneumoniae and Influenza Infections. Streptococcus pneumoniae (S.p.) is a major cause of morbidity and mortality worldwide. It is a major cause of community-acquired pneumonia (CAP) and also considered as a significant cause of a secondary infection associated with influenza virus infections. It is unclear why the mortality rate remains very high at an early stage. We recently found that CYLD plays a critical role in potentiating the S. pneumoniae-induced lethality. We are currently focusing on investigating the molecular targets and the underlying signaling mechanisms by which CYLD regulates S. pneumoniae-induced lethality.
 
Regulation of Mucus Overproduction in Bacterial Infections. Mucus overproduction is a hallmark of upper respiratory tract infections. How mucus is up-regulated remains largely unknown. We recently have identified several positive signaling pathways involved in mucus overproduction. We are currently focusing on determining the negative regulators involved in preventing overactive mucus overproduction and further exploring their translational potential.
 

Development of Novel Therapeutic Agents for Inflammatory and Infectious Diseases. Taking advantage of drug repositioning strategy, we recently discovered that Vinpocetine, a well-known natural product, acts as a potent anti-inflammatory agent. Vinpocetine was originally discovered nearly 30 years ago and has been approved for other clinical applications. Its already approved excellent safety and toxicity profile will significantly reduce clinical trial risk and time as well as the cost for drug development. We are currently working on further developing Vinpocetine into an anti-inflammatory therapeutic agent. In addition, we are also working on developing novel therapeutic agents for inhibiting mucus overproduction and reducing lethality.

Why Georgia?

• The strategic vision, the commitment and the unique support of Georgia Research Alliance andGeorgia State University to builda premier center for inflammation research and education

• The excellent opportunity and environment at Georgia State University for interdisciplinary collaboration

The highly supportive entrepreneurial environment to translate the laboratory discoveries into clinical applications


Other Georgia State University Eminent Scholars

James C. Cox , Ph.D. Experimental Economics
Julia Hilliard , Ph.D. Molecular Biotechnology
Jian-Dong Li , M.D., Ph.D. Inflammation and Immunity
Lars Mathiassen , Ph.D. Business Process Innovation
Binghe Wang , Ph.D. Drug Discovery and New Diagnostics
Peng George Wang , Ph.D. Chemical Glycobiology



 


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