The word “inflammation” is at the forefront of many chronic diseases affecting humans, including cancers, diabetes, obesity, metabolic syndrome, cardiovascular diseases, arthritis, and others. Historical use of the word inflammation was restricted to what we understood about acute innate responses to localized tissue damage and pathogen entry across anatomical barriers, and we understood chronic inflammation in terms of severe long term disease outcomes. In recent years the biological processes involved in inflammation have been revealed in surprising circumstances such as normal embryonic development, neurodevelopment, tissue regeneration, and in stressful conditions such as starvation, sleep deprivation, shivering thermogenesis, and other cases we may collectively refer to as physiological inflammation. Physiological inflammation is neither acute nor chronic, but rather meta-inflammatory. Mechanistically, these events are associated with metabolic disorders involving reprograming (polarizing) cells of the immune system towards new steady state responses following external and internal triggers. These triggers involve the loss of structure (e.g., altered gut epithelial structure and commensal microbiome), followed by loss of function (e.g., malabsorption of nutrients, altered peristalsis), and ultimately the loss of regulation (e.g., new steady state of lowered function and/or metabolism and dysbiosis of normal microflora). Moreover, a role of the unfolded protein response (UPR) in driving meta-inflammation is now appreciated. To understand and treat various diseases associated with inflammation, there has been much attention on anti-inflammatory small molecules that target key events during inflammatory processes. Several promising drug candidates are derived from natural products or repurposed drugs approved for other diseases. Some of these candidate drugs are active through pathways similar to known strong immunotoxic compounds such as PAHs, TCDD, PCBs, PFCs, and synthetic phenolic antioxidants to name a few. Thus, the toxic effects of many environmental contaminants may be associated with meta- and chronic inflammation, and at the forefront of these toxic responses is the reticuloendothelial-system (RES), also known as the mononuclear phagocytic system (MPS), involving macrophages – key players in inflammation. With environmental species such as fish and wildlife, the environment contains not only contaminants of interest, but also the local microbial consortium, and these interactions may lead to a state of inflammatory toxicity.
About the Speaker: Dr. Charles Rice received his B.S. in Biology Education at Virginia Commonwealth University, followed by a M.S. in Biology, also from Virginia Commonwealth University. His Ph.D. was obtained from the College of William & Mary, with a research focus on comparative immunology and immunopharmacology/toxicology. His work in immunology continued with a post-doctoral fellowship in brain tumor immunology at the Medical College of VA, where he was funded by the American Brain Tumor Association. Dr. Rice was then on the faculty of the College of Veterinary Medicine at Mississippi State University, where he continued in tumor immunology, environmental immunotoxicology, and began his interests in inflammation and its role in chronic diseases. Rice has been funded by NIH, EPA, NOAA, and various Foundations, including present funding from the Self-Regional Healthcare Human Genetics Research Program to investigate the possible role of inflammation in Autism Spectrum Disorders. Dr. Rice is recognized as an expert in the generation, development, and application of monoclonal antibodies for novel therapeutic approaches to several diseases impacting human health, fish, and wildlife.
Thursday, May 5, 12:00-1:15 pm Eastern
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